@article{kisler_anti-malaria_2023,
	title = {Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating {PICALM} at the blood-brain barrier},
	volume = {18},
	issn = {1750-1326},
	doi = {10.1186/s13024-023-00597-5},
	abstract = {BACKGROUND: PICALM is one of the most significant susceptibility factors for Alzheimer's disease (AD). In humans and mice, PICALM is highly expressed in brain endothelium. PICALM endothelial levels are reduced in AD brains. PICALM controls several steps in Aβ transcytosis across the blood-brain barrier (BBB). Its loss from brain endothelium in mice diminishes Aβ clearance at the BBB, which worsens Aβ pathology, but is reversible by endothelial PICALM re-expression. Thus, increasing PICALM at the BBB holds potential to slow down development of Aβ pathology.
METHODS: To identify a drug that could increase PICALM expression, we screened a library of 2007 FDA-approved drugs in HEK293t cells expressing luciferase driven by a human PICALM promoter, followed by a secondary mRNA screen in human Eahy926 endothelial cell line. In vivo studies with the lead hit were carried out in Picalm-deficient (Picalm+/-) mice, Picalm+/-; 5XFAD mice and Picalmlox/lox; Cdh5-Cre; 5XFAD mice with endothelial-specific Picalm knockout. We studied PICALM expression at the BBB, Aβ pathology and clearance from brain to blood, cerebral blood flow (CBF) responses, BBB integrity and behavior.
RESULTS: Our screen identified anti-malaria drug artesunate as the lead hit. Artesunate elevated PICALM mRNA and protein levels in Eahy926 endothelial cells and in vivo in brain capillaries of Picalm+/- mice by 2-3-fold. Artesunate treatment (32 mg/kg/day for 2 months) of 3-month old Picalm+/-; 5XFAD mice compared to vehicle increased brain capillary PICALM levels by 2-fold, and reduced Aβ42 and Aβ40 levels and Aβ and thioflavin S-load in the cortex and hippocampus, and vascular Aβ load by 34-51\%. Artesunate also increased circulating Aβ42 and Aβ40 levels by 2-fold confirming accelerated Aβ clearance from brain to blood. Consistent with reduced Aβ pathology, treatment of Picalm+/-; 5XFAD mice with artesunate improved CBF responses, BBB integrity and behavior on novel object location and recognition, burrowing and nesting. Endothelial-specific knockout of PICALM abolished all beneficial effects of artesunate in 5XFAD mice indicating that endothelial PICALM is required for its therapeutic effects.
CONCLUSIONS: Artesunate increases PICALM levels and Aβ clearance at the BBB which prevents development of Aβ pathology and functional deficits in mice and holds potential for translation to human AD.},
	language = {eng},
	number = {1},
	journal = {Molecular Neurodegeneration},
	author = {Kisler, Kassandra and Sagare, Abhay P. and Lazic, Divna and Bazzi, Sam and Lawson, Erica and Hsu, Ching-Ju and Wang, Yaoming and Ramanathan, Anita and Nelson, Amy R. and Zhao, Zhen and Zlokovic, Berislav V.},
	month = jan,
	year = {2023},
	pmid = {36707892},
	pmcid = {PMC9883925},
	keywords = {Alzheimer Disease, Alzheimer’s disease, Amyloid beta-Peptides, Amyloid-β, Animals, Antimalarials, Artesunate, Blood-Brain Barrier, Blood-brain barrier, Endothelial Cells, HEK293 Cells, Humans, Infant, Low Density Lipoprotein Receptor-Related Protein-1, Mice, Mice, Transgenic, Monomeric Clathrin Assembly Proteins, PICALM},
	pages = {7},
}

@article{xiao_vitro_2022,
	title = {In {Vitro} {ADME} and {Preclinical} {Pharmacokinetics} of {Ulotaront}, a {TAAR1}/5-{HT1A} {Receptor} {Agonist} for the {Treatment} of {Schizophrenia}},
	volume = {39},
	issn = {1573-904X},
	doi = {10.1007/s11095-022-03267-1},
	abstract = {PURPOSE: Ulotaront (SEP-363856) is a TAAR1 agonist with 5-HT1A agonist activity currently in clinical development for the treatment of schizophrenia. The objectives of the current study were to characterize the in vitro ADME properties, preclinical PK, and to evaluate the DDI potential of ulotaront and its major metabolite SEP-383103.
METHODS: Solubility, permeability, plasma protein binding, CYP inhibition and induction, transporter inhibition and uptake studies were conducted in vitro. Phenotyping studies were conducted using recombinant human CYPs and FMOs, human liver microsomes and human liver homogenates. Preclinical plasma and brain pharmacokinetics were determined after a single intraperitoneal, intravenous, and oral administration of ulotaront.
RESULTS: Ulotaront is a compound of high solubility, high permeability, and low binding to plasma proteins. Ulotaront metabolism is mediated via both NADPH-dependent and NADPH-independent pathways, with CYP2D6 as the major metabolizing enzyme. Ulotaront is an inducer of CYP2B6, and an inhibitor of CYP2D6, OCT1 and OCT2, while SEP-383103 is neither a CYP inducer nor a potent inhibitor of CYPs and human transporters. Ulotaront exhibits rapid absorption, greater than 70\% bioavailability, approximately 3.5 L/kg volume of distribution, 1.5-4 h half-life, 12-43 ml/min/kg clearance, and good penetration across the blood-brain barrier in preclinical species.
CONCLUSIONS: Ulotaront has been designated as a BCS1 compound by US FDA. The ability of ulotaront to penetrate the blood-brain barrier for CNS targeting has been demonstrated in mice and rats. The potential for ulotaront and SEP-383103 to act as perpetrators of CYP and transporter-mediated DDIs is predicted to be remote.},
	language = {eng},
	number = {5},
	journal = {Pharmaceutical Research},
	author = {Xiao, Guangqing and Chen, Yu-Luan and Dedic, Nina and Xie, Linghong and Koblan, Kenneth S. and Galluppi, Gerald R.},
	month = may,
	year = {2022},
	pmid = {35484370},
	keywords = {Animals, CYP2D6, Cytochrome P-450 CYP2D6, Cytochrome P-450 Enzyme System, Mice, Microsomes, Liver, NADP, Pharmaceutical Preparations, Rats, Receptor, Serotonin, 5-HT1A, Schizophrenia, TAAR1, blood–brain barrier, drug-drug interactions, phenotyping, ulotaront},
	pages = {837--850},
}

Paper  doi  abstract   bibtex   

@article{Kieswetter2022,
abstract = {Background: Previously, we evaluated the intracellular mycobactericidal activity of the minor groove binder, S-MGB-364 against the clinical Mycobacterium tuberculosis (Mtb) strain HN878 in macrophages. Objectives: To assess the mycobactericidal activity of S-MGB-364 in Mtb-infected mice. Further, we investigated a plausible DNA binding mechanism of action of S-MGB-364. Methods: The anti-TB and host immune effects of intranasal S-MGB-364 or S-MGB-364 encapsulated in non-ionic surfactant vesicles (NIV) were assessed in Mtb-infected mice by cfu enumeration, ELISA, histology, and flow cytometry. DNA binding was examined using native mass spectrometry and UV-vis thermal melt determination. S-MGB interference with DNA-centric biological events was assessed using a representative panel of Mtb and human topoisomerase I, and gyrase assays. Results: S-MGB-364 bound strongly to DNA as a dimer, significantly increasing the stability of the DNA:S-MGB complex compared with DNA alone. Moreover, S-MGB-364 inhibited the relaxation of Mtb topoisomerase I but not the human form. In macrophages, S-MGB-364 or S-MGB-364-NIV did not cause DNA damage as shown by the low $\gamma$-H2AX expression. Importantly, in the lungs, the intranasal administration of S-MGB-364 or S-MGB-364-NIV formulation in Mtb-infected mice was non-toxic and resulted in a 1 log cfu reduction in mycobacter-ial burden, reduced the expression of proinflammatory cytokines/chemokines, altered immune cell recruitment, and importantly reduced recruitment of neutrophils. Conclusions: Together, these data provide proof of concept for S-MGBs as novel anti-TB therapeutics in vivo.},
author = {Kieswetter, Nathan S and Ozturk, Mumin and Hlaka, Lerato and Chia, Julius Ebua and Nichol, Ryan J O and Cross, Jasmine M and McGee, Leah M C and Tyson-Hirst, Izaak and Beveridge, Rebecca and Brombacher, Frank and Carter, Katharine C and Suckling, Colin J and Scott, Fraser J and Guler, Reto},
doi = {10.1093/JAC/DKAC001},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Kieswetter et al. - 2022 - Intranasally administered S-MGB-364 displays antitubercular activity and modulates the host immune response t.pdf:pdf},
issn = {0305-7453},
journal = {Journal of Antimicrobial Chemotherapy},
keywords = {OA,antitubercular agents,chemical surfactants,chemokines,cytokine,dimers,dna,dna topoisomerases,enzyme-linked immunosorbent assay,flow cytometry,fund{\_}ack,histology,immune response,infections,intranasal administration,lung,macrophages,mass spectrometry,mice,mycobacterium tuberculosis,neutrophils,noninvasive ventilation,original,pharmacokinetics,proof of concept studies,pulmonary surfactants,tuberculosis,type i,vaccine information sheets,vesicle},
mendeley-tags = {OA,fund{\_}ack,original},
month = {jan},
number = {4},
pages = {1061--1071},
pmid = {35084027},
publisher = {Oxford University Press (OUP)},
title = {{Intranasally administered S-MGB-364 displays antitubercular activity and modulates the host immune response to \textit{Mycobacterium tuberculosis} infection}},
url = {https://academic.oup.com/jac/advance-article/doi/10.1093/jac/dkac001/6515318},
volume = {77},
year = {2022}
}

@article{chen_artemisinin_2020,
	title = {Artemisinin compounds sensitize cancer cells to ferroptosis by regulating iron homeostasis},
	volume = {27},
	issn = {1476-5403},
	doi = {10.1038/s41418-019-0352-3},
	abstract = {The antimalarial drug artemisinin and its derivatives have been explored as potential anticancer agents, but their underlying mechanisms are controversial. In this study, we found that artemisinin compounds can sensitize cancer cells to ferroptosis, a new form of programmed cell death driven by iron-dependent lipid peroxidation. Mechanistically, dihydroartemisinin (DAT) can induce lysosomal degradation of ferritin in an autophagy-independent manner, increasing the cellular free iron level and causing cells to become more sensitive to ferroptosis. Further, by associating with cellular free iron and thus stimulating the binding of iron-regulatory proteins (IRPs) with mRNA molecules containing iron-responsive element (IRE) sequences, DAT impinges on IRP/IRE-controlled iron homeostasis to further increase cellular free iron. Importantly, in both in vitro and a mouse xenograft model in which ferroptosis was triggered in cancer cells by the inducible knockout of GPX4, we found that DAT can augment GPX4 inhibition-induced ferroptosis in a cohort of cancer cells that are otherwise highly resistant to ferroptosis. Collectively, artemisinin compounds can sensitize cells to ferroptosis by regulating cellular iron homeostasis. Our findings can be exploited clinically to enhance the effect of future ferroptosis-inducing cancer therapies.},
	language = {eng},
	number = {1},
	journal = {Cell Death and Differentiation},
	author = {Chen, Guo-Qing and Benthani, Fahad A. and Wu, Jiao and Liang, Deguang and Bian, Zhao-Xiang and Jiang, Xuejun},
	month = jan,
	year = {2020},
	pmid = {31114026},
	pmcid = {PMC7205875},
	keywords = {Animals, Antineoplastic Agents, Artemisinins, Autophagy, Cell Line, Tumor, Female, Ferroptosis, Homeostasis, Humans, Iron, Iron-Regulatory Proteins, Lysosomes, Mice, Nude, Neoplasms, Response Elements},
	pages = {242--254},
}

@article{raina_gelatin-_2018,
	title = {Gelatin- hydroxyapatite- calcium sulphate based biomaterial for long term sustained delivery of bone morphogenic protein-2 and zoledronic acid for increased bone formation: {In}-vitro and in-vivo carrier properties},
	volume = {272},
	issn = {1873-4995},
	doi = {10.1016/j.jconrel.2018.01.006},
	abstract = {In this study, a novel macroporous composite biomaterial consisting of gelatin-hydroxyapatite-calcium sulphate for delivery of bone morphogenic protein-2 (rhBMP-2) and zoledronic acid (ZA) has been developed. The biomaterial scaffold has a porous structure and functionalization of the scaffold with rhBMP-2 induces osteogenic differentiation of MC3T3-e1 cells seen by a significant increase in biochemical and genetic markers of osteoblastic differentiation. In-vivo muscle pouch experiments showed higher mineralization using scaffold+rhBMP-2 when compared to an approved absorbable collagen sponge (ACS)+rhBMP-2 as verified by micro-CT. Co-delivery of rhBMP-2+ZA via the novel scaffold enabled a reduction in the effective rhBMP-2 doses. The presence of tartrate resistant acid phosphatase staining in the rhBMP-2 group indicates osteoclastic resorption, which could be stalled by adding ZA, which by speculation could explain the net increase in mineralization. The new scaffold allowed for slow release of rhBMP-2 in-vitro (3.3±0.1\%) after 4weeks. Using single photon emission computed tomography (SPECT), the release kinetics of 125I-rhBMP-2 in-vivo was followed for 4weeks and a total of 65.3±15.2\% 125I-rhBMP-2 was released from the scaffolds. In-vitro 14C-ZA release curve shows an initial burst release on day 1 (8.8±0.7\%) followed by a slow release during the following 4weeks (13±0.1\%). In-vivo, an initial release of 43.2±7.6\% of 14C-ZA was detected after 1day, after which the scaffold retained the remaining ZA during 4-weeks. Taken together, our results show that the developed biomaterial is an efficient carrier for spatio-temporal delivery of rhBMP-2 and ZA leading to increased bone formation compared to commercially available carrier for rhBMP-2.},
	language = {eng},
	journal = {Journal of Controlled Release: Official Journal of the Controlled Release Society},
	author = {Raina, Deepak Bushan and Larsson, David and Mrkonjic, Filip and Isaksson, Hanna and Kumar, Ashok and Lidgren, Lars and Tägil, Magnus},
	year = {2018},
	pmid = {29329716},
	keywords = {Animals, Biocompatible Materials, Bone Density Conservation Agents, Bone Morphogenetic Protein 2, Bone morphogenic protein (BMP), Calcium Sulfate, Cell Line, Cell Survival, Cryogels, Delayed-Action Preparations, Durapatite, Gelatin, Hydroxyapatite, In-vivo BMP release, In-vivo ZA release, Male, Mice, Osteogenesis, Rats, Sprague-Dawley, Recombinant Proteins, Transforming Growth Factor beta, Zoledronic Acid, Zoledronic acid (ZA)},
	pages = {83--96},
}

@article{kisler_pericyte_2017,
	title = {Pericyte degeneration leads to neurovascular uncoupling and limits oxygen supply to brain},
	volume = {20},
	issn = {1546-1726},
	doi = {10.1038/nn.4489},
	abstract = {Pericytes are perivascular mural cells of brain capillaries. They are positioned centrally in the neurovascular unit between endothelial cells, astrocytes and neurons. This position allows them to regulate key neurovascular functions of the brain. The role of pericytes in the regulation of cerebral blood flow (CBF) and neurovascular coupling remains, however, under debate. Using loss-of-function pericyte-deficient mice, here we show that pericyte degeneration diminishes global and individual capillary CBF responses to neuronal stimuli, resulting in neurovascular uncoupling, reduced oxygen supply to the brain and metabolic stress. Neurovascular deficits lead over time to impaired neuronal excitability and neurodegenerative changes. Thus, pericyte degeneration as seen in neurological disorders such as Alzheimer's disease may contribute to neurovascular dysfunction and neurodegeneration associated with human disease.},
	language = {eng},
	number = {3},
	journal = {Nature Neuroscience},
	author = {Kisler, Kassandra and Nelson, Amy R. and Rege, Sanket V. and Ramanathan, Anita and Wang, Yaoming and Ahuja, Ashim and Lazic, Divna and Tsai, Philbert S. and Zhao, Zhen and Zhou, Yi and Boas, David A. and Sakadžić, Sava and Zlokovic, Berislav V.},
	month = mar,
	year = {2017},
	pmid = {28135240},
	pmcid = {PMC5323291},
	keywords = {Animals, Brain, Capillaries, Cell Death, Female, Homeodomain Proteins, Male, Mice, Mice, Transgenic, Nerve Degeneration, Neurons, Oxygen, Pericytes, Receptor, Platelet-Derived Growth Factor beta, Stress, Physiological, Vasodilation},
	pages = {406--416},
}

@article{laurent_hippocampal_2017,
	title = {Hippocampal {T} cell infiltration promotes neuroinflammation and cognitive decline in a mouse model of tauopathy},
	volume = {140},
	issn = {1460-2156},
	doi = {10.1093/brain/aww270},
	abstract = {Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms. Neuroinflammatory changes are thought to be major contributors to Alzheimer's disease pathophysiology, even if their precise role still remains largely debated. Notably, to what extent immune responses contribute to cognitive impairments promoted by tau pathology remains poorly understood. To address this question, we took advantage of the THY-Tau22 mouse model that progressively develops hippocampal tau pathology paralleling cognitive deficits and reappraised the interrelationship between tau pathology and brain immune responses. In addition to conventional astroglial and microglial responses, we identified a CD8-positive T cell infiltration in the hippocampus of tau transgenic mice associated with an early chemokine response, notably involving CCL3. Interestingly, CD8-positive lymphocyte infiltration was also observed in the cortex of patients exhibiting frontemporal dementia with P301L tau mutation. To gain insights into the functional involvement of T cell infiltration in the pathophysiological development of tauopathy in THY-Tau22 mice, we chronically depleted T cells using anti-CD3 antibody. Such anti-CD3 treatment prevented hippocampal T cell infiltration in tau transgenic animals and reverted spatial memory deficits, in absence of tau pathology modulation. Altogether, these data support an instrumental role of hippocampal T cell infiltration in tau-driven pathophysiology and cognitive impairments in Alzheimer's disease and other tauopathies.},
	language = {eng},
	number = {1},
	journal = {Brain: A Journal of Neurology},
	author = {Laurent, Cyril and Dorothée, Guillaume and Hunot, Stéphane and Martin, Elodie and Monnet, Yann and Duchamp, Marie and Dong, Yuan and Légeron, François-Pierre and Leboucher, Antoine and Burnouf, Sylvie and Faivre, Emilie and Carvalho, Kévin and Caillierez, Raphaëlle and Zommer, Nadège and Demeyer, Dominique and Jouy, Nathalie and Sazdovitch, Veronique and Schraen-Maschke, Susanna and Delarasse, Cécile and Buée, Luc and Blum, David},
	month = jan,
	year = {2017},
	pmid = {27818384},
	pmcid = {PMC5382942},
	keywords = {Aged, Hippocampus, Humans, Cerebral Cortex, Middle Aged, Animals, frontotemporal lobar degeneration, Tauopathies, Mice, Mice, Inbred C57BL, Mice, Transgenic, Disease Models, Animal, Cognitive Dysfunction, tauopathy, CD3 Complex, Antibodies, Inflammation, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, chemokines, Chemokines, neuroinflammation, T cells},
	pages = {184--200}
}

@article{xu_csa13_2017,
	title = {{CSA13} inhibits colitis-associated intestinal fibrosis via a formyl peptide receptor like-1 mediated {HMG}-{CoA} reductase pathway},
	volume = {7},
	issn = {2045-2322},
	doi = {10.1038/s41598-017-16753-z},
	abstract = {Many Crohn's disease (CD) patients develop intestinal strictures, which are difficult to prevent and treat. Cationic steroid antimicrobial 13 (CSA13) shares cationic nature and antimicrobial function with antimicrobial peptide cathelicidin. As many functions of cathelicidin are mediated through formyl peptide receptor-like 1 (FPRL1), we hypothesize that CSA13 mediates anti-fibrogenic effects via FPRL1. Human intestinal biopsies were used in clinical data analysis. Chronic trinitrobenzene sulfonic acid (TNBS) colitis-associated intestinal fibrosis mouse model with the administration of CSA13 was used. Colonic FPRL1 mRNA expression was positively correlated with the histology scores of inflammatory bowel disease patients. In CD patients, colonic FPRL1 mRNA was positively correlated with intestinal stricture. CSA13 administration ameliorated intestinal fibrosis without influencing intestinal microbiota. Inhibition of FPRL1, but not suppression of intestinal microbiota, reversed these protective effects of CSA13. Metabolomic analysis indicated increased fecal mevalonate levels in the TNBS-treated mice, which were reduced by the CSA13 administration. CSA13 inhibited colonic HMG-CoA reductase activity in an FPRL1-dependent manner. Mevalonate reversed the anti-fibrogenic effect of CSA13. The increased colonic FPRL1 expression is associated with severe mucosal disease activity and intestinal stricture. CSA13 inhibits intestinal fibrosis via FPRL1-dependent modulation of HMG-CoA reductase pathway.},
	language = {eng},
	number = {1},
	journal = {Scientific Reports},
	author = {Xu, Chunlan and Ghali, Sally and Wang, Jiani and Shih, David Q. and Ortiz, Christina and Mussatto, Caroline C. and Lee, Elaine C. and Tran, Diana H. and Jacobs, Jonathan P. and Lagishetty, Venu and Fleshner, Phillip and Robbins, Lori and Vu, Michelle and Hing, Tressia C. and McGovern, Dermot P. B. and Koon, Hon Wai},
	year = {2017},
	pmid = {29180648},
	pmcid = {PMC5703874},
	keywords = {Animals, Anti-Bacterial Agents, Colitis, Disease Models, Animal, Fibrosis, Gastrointestinal Microbiome, Gene Expression, Humans, Hydroxymethylglutaryl CoA Reductases, Inflammatory Bowel Diseases, Intestinal Mucosa, Metabolome, Metabolomics, Mice, RNA, Messenger, Receptors, Formyl Peptide, Receptors, Lipoxin, Signal Transduction},
	pages = {16351},
}

Website  abstract   bibtex   

@article{
 title = {The National Center for Genome Analysis Support},
 type = {article},
 year = {2017},
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 keywords = {DvlFinal,PY1,PY2,PY3,PY4,PY5,PY6,PY7,PY8,py8},
 pages = {e0165395},
 volume = {11},
 websites = {https://itnews.iu.edu/articles/2018/Teaching HPC and genomics side-by-side.php,https://itnews.iu.edu/articles/2016/highlight-students-and-faculty-receive-valuable-training-at-environmental-genomics-workshop.php,https://itnews.iu.edu/articles/2017/iu-proje},
 month = {1},
 publisher = {Plant and Animal Genomics 2018},
 day = {15},
 city = {Bloomington, Indiana},
 series = {XSEDE '15},
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 last_modified = {2020-02-26T20:18:12.515Z},
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 citation_key = {Ganote2018},
 source_type = {article},
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 country = {England},
 patent_owner = {NLM},
 notes = {<b>From Duplicate 1 (<i>The National Center for Genome Analysis Support</i> - Sanders, Sheri A.; Papudeshi, Bhavya Nalagampalli; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Mansfield, Charles; Tseng, Chi Yen; Custer, Thomas; Custer, Christine; Matson, Cole; Johri, Parul; Marinov, Georgi K; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Lynch, Michael; Cai, Jasmine X.; Weathers, Jania G.; Leffler, Haley; Ganapaneni, Sruthi; Papudeshi, Bhavya; Sanders, Sheri; Doak, Thomas G; Sanders, Sheri A.; Papudeshi, Bhavya Nalagampalli; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Chafin, Tyler; Reshetnikov, Andrey; Sokolov, Sergey; Pummil, Jeff; Douglas, Michael Marlis; Douglas, Michael Marlis; Sander, Sheri; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Leffler, Haley; Ganapaneni, Sruthi; Papudeshi, Bhavya Nalagampalli; Ganote, CL Carrie L.; Sanders, Sheri A.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Cai, Jasmine X; Weathers, Jania G; Leffler, Haley; Ganapaneni, Sruthi; Papudeshi, Bhavya Nalagampalli; Sanders, Sheri A.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Foran, Eliza G.; Suggs, Evan D.; Underwood, Tenecious A.; Snapp-Childs, Winona; Sanders, Sheri A; Foran, Eliza; Anderson, Jazzly; Slayton, Thomas; Guido, Emmanuel; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Sanders, Sheri A.; Russell, Kristin; Papudeshi, Bhavya Nalagampalli; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Papudeshi, Bhavya Nalagampalli; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Podicheti, Ram; Yang, Tianhong; Fang, Lingling; Jayanthi, Srinivas; Rajan, Gayathri; Kumar, Thallapuranam Krishnaswarmy Suresh; Medina-Bolivar, Fabricio; Mockaitis, Keithanne; Sanders, Sheri A.; Jayanthi, Srinivas; Rajan, Gayathri; Podicheti, Ram; Thallapuranam, Suresh Kumar; Mockaitis, Keithanne; Medina-Bolivar, Fabricio; Long, Hongan., Doak, G, Thomas., Lynch, Michael.; Michaels, Scott D. SD D (; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Michaels, Scott D. SD D (; Ganote, CL Carrie L.; Papudeshi, Bhavya Nalagampalli; Sanders, Sheri A.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Behringer, Megan G; Choi, Brian I; Miller, Samuel F; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Karty, Jonathan A; Guo, Wanfeng; Lynch, Michael; Anderson, Jazzly; Slayton, Thomas; Guido, Emmanuel; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Sanders, Sheri A.; Ganote, CL Carrie L.; Mendes, Fabio; Henschel, Robert; Hahn, Matthew; Fulton, Ben; Papudeshi, Bhavya Nalagampalli; Sanders, Sheri A.; Ganote, CL Carrie L.; Fischer, Jeremy; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Wernert, Julie; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Sanders, Sheri A.; Ganote, CL Carrie L.; Papudeshi, Bhavya Nalagampalli; Sanders, Sheri A.; Papudeshi, Bhavya Nalagampalli; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Sanders, Sheri A.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Mockaitis, Keithanne; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Hancock, David Y.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Wernert, Julie; Miller, Therese; Bhavya, Papudeshi; Sanders, Sheri A.; Ganote, CL Carrie L.; Blood, Philip D. Phillip D.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Haas, Brian BJ; Dobin, Alexander; Stransky, Nicolas; Li, Bo; Yang, Xiao; Tickle, Timothy; Bankapur, Asma; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Pochet, Natalie; Sun, Jing; Wu, Catherine; Gingeras, Thomas R.; Regev, Aviv; Doak Craig A Stewart Scott D Michaels, Thomas G; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Michaels, Scott D. SD D (; Papudeshi, Bhavya Nalagampalli; Haggerty, J. Matthew; Doane, Michael; Morris, Megan M.; Walsh, Kevin; Beattie, Douglas T.; Pande, Dnyanada; Zaeri, Parisa; Silva, Genivaldo G.Z.; Thompson, Fabiano; Edwards, Robert A.; Dinsdale, Elizabeth A.; Sanders, Sheri A.; Pfrender, Michael E; Blood, Philip D. Phillip D.; Ganote, CL Carrie L.; Sanders, Sheri A.; Papudeshi, Bhavya Nalagampalli; Blood, Philip D. Phillip D.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Klegarth, A R; Sanders, Sheri A.; Gloss, A D; Lane‐deGraaf, K E; Jones‐Engel, L; Fuentes, A; Hollocher, H; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Wernert, Julie; Hancock, David Y.; Miller, Therese; Plale, Beth; Welch, Von; Pierce, Marlon; Fox, Geoffrey C.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Hancock, David Y.; Henschel, Robert; Link, Matthew R.; Miller, Therese; Wernert, Eric; Boyles, Michael J.; Fulton, Ben; Weakley, Le Mai; Ping, Robert J; Gniady, Tassie; Snapp-Childs, Winona; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Blood, Philip D. Phillip D.; Sanders, Sheri A.; Stewart, Craig CA A Craig A.; Michaels, Scott D. SD D (; Ackerman, Matthew S; Johri, Parul; Spitze, Ken; Xu, Sen; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Young, Kimberly; Lynch, Michael; Krenek, Sascha; Marinov, Georgi K; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Berendonk, Thomas U; Lynch, Michael; Ganote, CL Carrie L.; Sanders, Sheri A.; Hallock, Barb; Blood, Philip D. Phillip D.; Ganote, CL Carrie L.; Sanders, Sheri A.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Brokaw, Cicada; Bhavya, N P; Haas, Brian BJ; Ganote, CL Carrie L.; Zaila, Kassandra E.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ellerbrock, Hannah; Tung, Che Huang; Martins, Mauricio L.; Kolbin, Daniel; Yao, Meng Chao; Cassidy-Hanley, Donna M.; Clark, Theodore G.; Chang, Wei-Jen Jen; Sczyrba, Alexander; Hofmann, Peter; Belmann, Peter; Koslicki, David; Janssen, Stefan; Droege, Johannes; Gregor, Ivan; Majda, Stephan; Fiedler, Jessika; Dahms, Eik; Bremges, Andreas; Fritz, Adrian; Garrido-Oter, Ruben; Jorgensen, Tue S; Shapiro, Nicole; Blood, Philip D. Phillip D.; Gurevich, Alexey; Bai, Yang; Turaev, Dmitrij; DeMaere, Matthew Z; Chikhi, Rayan; Nagarajan, Niranjan; Quince, Christopher; Hansen, Lars H; Sorensen, Soren J; Chia, Burton K H; Denis, Bertrand; Froula, Jeff L; Wang, Zhong; Egan, Robert; Kang, Dongwan D; Cook, Jeffrey J; Deltel, Charles; Beckstette, Michael; Lemaitre, Claire; Peterlongo, Pierre; Rizk, Guillaume; Lavenier, Dominique; Wu, Yu-Wei Ye; Singer, Steven W; Jain, Chirag; Strous, Marc; Klingenberg, Heiner; Meinicke, Peter; Barton, Michael; Lingner, Thomas; Lin, Hsin-Hung; Liao, Yu-Chieh; Gueiros, Genivaldo; Cuevas, Daniel A; Edwards, Robert A.; Saha, Surya; Piro, Vitor C; Renard, Bernhard Y; Pop, Mihai; Klenk, Hans-Peter; Goeker, Markus; Kyrpides, Nikos; Woyke, Tanja; Vorholt, Julia A; Schulze-Lefert, Paul; Rubin, Edward M; Darling, Aaron E; Rattei, Thomas; McHardy, Alice C; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Tydecks, Laura; Bremerich, Vanessa; Jentschke, Ilona; Likens, Gene E.; Tockner, Klement; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Blood, Philip D. Phillip D.; Ganote, CL Carrie L.; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ghaffari, Noushin; Abante, Jordi; Singh, Raminder; Blood, Philip D. Phillip D.; Johnson, Charles D.; Kucukyildirim, Sibel; Long, Hongan; Sung, Way; Miller, Samuel F; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Lynch, Michael; Chandran, Uma R; Medvedeva, Olga P; Barmada, M Michael; Blood, Philip D. Phillip D.; Chakka, Anish; Luthra, Soumya; Ferreira, Antonio; Wong, Kim F; Lee, Adrian V.; Zhang, Zhihui; Budden, Robert; Scott, J Ray; Berndt, Annerose; Berg, Jeremy M; Jacobson, Rebecca S; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Stewart, Craig CA A Craig A.; Michaels, Scott D. SD D (; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Lee, Heewook; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Popodi, Ellen; Foster, Patricia L; Tang, Haixu; Sanders, Sheri A.; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Blood, Philip D. Phillip D.; Ganote, CL Carrie L.; Sanders, Sheri A.; Nimkulrat, Sutichot; Lee, Heewook; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ye, Yuzhen; Ntai, I; LeDuc, RD D Richard D.; Fellers, RT; Neeman, Henry; Bergstrom, Aaron; Brunson, Dana; Ganote, CL Carrie L.; Gray, Zane; Guilfoos, Brian; Kalescky, Robert; Lemley, Evan; Moore, Brian G; Ramadugu, Sai Kumar; Romanella, Alana; Rush, Johnathan; Sherman, Andrew H; Stengel, Brian; Voss, Dan; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Barnett, William K WK William K.; Seetharam, Arun; Gomez, Antonio; Purcell, Catherine M; Hyde, John R; Blood, Philip D. Phillip D.; Severin, Andrew J; Uy, KL; LeDuc, RD D Richard D.; Ganote, CL Carrie L.; Wang, M; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ye, Yuzhen; Ganote, CL Carrie L.; Hallock, Barb; Lee, F J; Rusch, D B; Stewart, F J; Zhang, Yujia Yuehua; Kong, Weijing; Gao, Yang; Liu, Xiaoyan; Gao, Kai; Xie, Han; Wu, Yu-Wei Ye; Zhang, Yujia Yuehua; Wang, Jingmin; Gao, Feng; Wu, Xiru; Jiang, Yuwu; Youssef, N. H.; Couger, M. Brian; Struchtemeyer, C. G.; Liggenstoffer, A. S.; Prade, R. A.; Najar, F. Z.; Atiyeh, H. K.; Wilkins, M. R.; Elshahed, M. S.; Wu, Zhiqiang; Yang, Li; Ren, Xianwen; He, Guimei; Zhang, Junpeng Jin; Yang, Jian; Qian, Zhaohui; Dong, Jie; Sun, Lilian; Zhu, Yafang; Du, Jiang; Yang, Fan; Zhang, Shuyi; Jin, Qi; Uy, KL; LeDuc, RD D Richard D.; Ganote, CL Carrie L.; Tarpy, David R; Mattila, Heather R; Newton, ILG Irene L G; Subramanian, Sandeep; Chaparala, Srilakshmi; Avali, Viji; Ganapathiraju, Madhavi K.; Stanton-Geddes, John; Paape, Timothy; Epstein, Brendan; Briskine, Roman; Yoder, Jeremy; Mudge, Joann; Bharti, Arvind K.; Farmer, Andrew D.; Zhou, Peng; Denny, Roxanne; May, Gregory D. Gemma E.; Erlandson, Stephanie; Yakub, Mohammed; Sugawara, Masayuki; Sadowsky, Michael J.; Young, Nevin D.; Tiffin, Peter; Sousounis, Konstantinos; Qi, Feng; Yadav, Manisha C; Millan, Jose Luis; Toyama, Fubito; Chiba, Chikafumi; Eguchi, Yukiko; Eguchi, Goro; Tsonis, Panagiotis A; Roncalli, Vittoria; Cieslak, MC Matthew C MC; Lenz, PH Petra H.; Rokop, Z P; Horton, Melissa A; Newton, ILG Irene L G; Raborn, RT Taylor; Spitze, Ken; Brendel, Volker P VP; Lynch, Michael; Qin, Xiaomei; Huang, Sheng; Liu, Yanqing; Bian, Mingdi; Shi, Wuliang; Zuo, Zecheng; Yang, Zhenming; Pipes, Lenore; Li, Sheng; Bozinoski, Marjan; Palermo, Robert E.; Peng, Xinxia; Blood, Philip D. Phillip D.; Kelly, Sara; Weiss, Jeffrey M.; Thierry-Mieg, Jean; Thierry-Mieg, Danielle; Zumbo, Paul; Chen, Ronghua; Schroth, Gary P.; Mason, Christopher E.; Katze, Michael G.; Phuong, Mark Anthony; Mahardika, Gusti N; Peterson, M; Malloy, J; Buonaccorsi, V; Marden, J; Petersen, Isaac T.; Bates, John E.; Dodge, Kenneth A.; Lansford, Jennifer E.; Pettit, Gregory S.; Peng, Xinxia; Pipes, Lenore; Xiong, Hao; Green, Richard R.; Jones, Daniel C.; Ruzzo, Walter L.; Schroth, Gary P.; Mason, Christopher E.; Palermo, Robert E.; Katze, Michael G.; Orsini, Luisa; Gilbert, Donald; Podicheti, Ram; Jansen, Mieke; Brown, James B.; Solari, Omid Shams; Spanier, Katina I; Colbourne, John K; Rush, Douglas; Decaestecker, Ellen; Asselman, Jana; De Schamphelaere, Karel A C; Ebert, Dieter; Haag, Christoph R; Kvist, Jouni; Laforsch, Christian; Petrusek, Adam; Beckerman, Andrew P; Little, Tom J; Chaturvedi, Anurag; Pfrender, Michael E; De Meester, Luc; Frilander, Mikko J; Newton, ILG Irene L G; Sheehan, KB Kathy B; Motamayor, Juan C; Mockaitis, Keithanne; Schmutz, Jeremy; Haiminen, Niina; III, Donald Livingstone; Cornejo, Omar; Findley, Seth D; Zheng, Ping; Utro, Filippo; Royaert, Stefan; Saski, Christopher; Jenkins, Jerry; Podicheti, Ram; Zhao, Meixia; Scheffler, Brian E; Stack, Joseph C; Feltus, Frank A; Mustiga, Guiliana M; Amores, Freddy; Phillips, Wilbert; Marelli, Jean Philippe; May, Gregory D. Gemma E.; Shapiro, Howard; Ma, Jianxin; Bustamante, Carlos D; Schnell, Raymond J; Main, Dorrie; Gilbert, Donald; Parida, Laxmi; Kuhn, DN David N; McGrath, Casey L. CL; Gout, JF Jean-Francois JF; Johri, Parul; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Yanagi, Akira; Lynch, Michael; Martínez, Teresa; Ropelewski, Alexander J; González-Mendez, Ricardo; Vázquez, Guillermo J; Robledo, Iraida E.; Martinez, Teresa; Aquino, Edna E.; Robledo, Iraida E.; Martinez, Idali; Vazquez, Guillermo J.; Aquino, Edna E.; Robledo, Iraida E.; Lipovich, Leonard; Hou, Zhuo-Cheng; Jia, Hui; Sinkler, Christopher; McGowen, Michael; Sterner, Kirstin N.; Weckle, Amy; Sugalski, Amara B.; Pipes, Lenore; Gatti, Domenico L.; Mason, Christopher E.; Sherwood, Chet C.; Hof, Patrick R.; Kuzawa, Christopher W.; Grossman, Lawrence I.; Goodman, Morris; Wildman, Derek E.; Kuhn, DN David N; Dillon, NL; Innes, DJ; Wu, Le-Shin S LS; Krishnakumar, Raga; Chen, Amy F; Pantovich, Marisol G; Danial, Muhammad; Parchem, Ronald J; Labosky, Patricia A; Blelloch, Robert; Jin, M; Bothfeld, W; Austin, S; Sato, TK; Reau, A La; Huth, Troy J; Place, Sean P; Horton, Melissa A; Oliver, Randy; Newton, ILG Irene L G; Gulia-Nuss, Monika; Nuss, Andrew B; Meyer, Jason M; Sonenshine, Daniel E; Roe, R Michael; Waterhouse, Robert M; Sattelle, David B; de la Fuente, Jose; Ribeiro, Jose M; Megy, Karine; Thimmapuram, Jyothi; Miller, Jason R; Walenz, Brian P; Koren, Sergey; Hostetler, Jessica B; Thiagarajan, Mathangi; Joardar, Vinita S; Hannick, Linda I; Bidwell, Shelby; Hammond, Martin P; Young, Sarah; Zeng, Qiandong; Abrudan, Jenica L; Almeida, Francisca C; Ayllon, Nieves; Bhide, Ketaki; Bissinger, Brooke W; Bonzon-Kulichenko, Elena; Buckingham, Steven D; Caffrey, Daniel R; Caimano, Melissa J; Croset, Vincent; Driscoll, Timothy; Gilbert, Donald; Gillespie, Joseph J; Giraldo-Calderon, Gloria I; Grabowski, Jeffrey M; Jiang, David; Khalil, Sayed M S; Kim, Donghun; Kocan, Katherine M; Koci, Juraj; Kuhn, Richard J; Kurtti, Timothy J; Lees, Kristin; Lang, Emma G; Kennedy, Ryan C; Kwon, Hyeogsun; Perera, Rushika; Qi, Yumin; Radolf, Justin D; Sakamoto, Joyce M; Sanchez-Gracia, Alejandro; Severo, Maiara S; Silverman, Neal; Simo, Ladislav; Tojo, Marta; Tornador, Cristian; Van Zee, Janice P; Vazquez, Jesus; Vieira, Filipe G; Villar, Margarita; Wespiser, Adam R; Yang, Yunlong; Zhu, Jiwei; Arensburger, Peter; Pietrantonio, Patricia V; Barker, Stephen C; Shao, Renfu; Zdobnov, Evgeny M; Hauser, Frank; Grimmelikhuijzen, Cornelis J P; Park, Yoonseong; Rozas, Julio; Benton, Richard; Pedra, Joao H F; Nelson, David R; Unger, Maria F; Tubio, Jose M C; Tu, Zhijian; Robertson, Hugh M; Shumway, Martin; Sutton, Granger; Wortman, Jennifer R; Lawson, Daniel; Wikel, Stephen K; Nene, Vishvanath M; Fraser, Claire M; Collins, Frank H; Birren, Bruce; Nelson, Karen E; Caler, Elisabet; Hill, Catherine A; Ghaffari, Noushin; Sanchez-Flores, Alejandro; Doan, Ryan; Garcia-Orozco, Karina D.; Chen, Patricia L.; Ochoa-Leyva, Adrian; Lopez-Zavala, Alonso A.; Carrasco, J. Salvador; Hong, Chris; Brieba, Luis G.; Rudiño-Piñera, Enrique; Blood, Philip D. Phillip D.; Sawyer, Jason E.; Johnson, Charles D.; Dindot, Scott V.; Sotelo-Mundo, Rogerio R.; Criscitiello, Michael F.; Gao, Kai; Tankovic, Anel; Zhang, Yujia Yuehua; Kusumoto, Hirofumi; Zhang, Junpeng Jin; Chen, Wenjuan; XiangWei, Wenshu; Shaulsky, Gil H.; Hu, Chun; Traynelis, Stephen F.; Yuan, Hongjie; Jiang, Yuwu; Fergus, Daniel J; Feng, Ni Y; Bass, Andrew H; Fergus, Daniel J; Bass, Andrew H; Duncan, Rebecca P; Feng, Honglin; Nguyen, Douglas M; Wilson, Alex C C; Darris, Carl E; Tyus, James E; Kelley, Gary; Ropelewski, Alexander J; Nicholas, Hugh B; Wang, Xiaofei; Nahashon, Samuel; Nahashon, Samuel; Couger, M. Brian; Pipes, Lenore; Squina, F; Boyd, Bret M.; Allen, Julie M.; Nguyen, Nam; Sweet, Andrew D.; Warnow, Tandy; Shapiro, Michael D.; Villa, Scott M.; Bush, Sarah E.; Clayton, Dale H.; Johnson, Kevin P.; Blood, Philip D. Phillip D.; Marcus, Shoshana; Schatz, Michael C.; Bahreini, Amir; Levine, Kevin; Santana-Santos, Lucas; Benos, Panayiotis V.; Wang, Peilu; Andersen, Courtney; Oesterreich, Steffi; Lee, Adrian V.; Armstrong, Eric J.; Stillman, Jonathon H.; Arafat, Ahmed; Jing, Peng; Ma, Yuping; Pu, Miao; Nan, Gai; Fang, He; Chen, Chen; Fei, Yin; Almada, Amalia A.; Tarrant, Ann M.; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Bao, G; Wang, M; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ye, Yuzhen; Barnett, William K WK William K.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Wu, Le-Shin S LS; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; LeDuc, RD D Richard D.; Vaughn, Matthew; Fonner, JM; Zhang, Quan; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ye, Yuzhen; Hallock, Barb; Ganote, CL Carrie L.; Pespeni, M; Hayashi, S; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Barnett, William K WK William K.; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Wegrzyn, J. L.; Liechty, J. D.; Stevens, K. A.; Wu, Le-Shin S LS; Loopstra, C. A.; Vasquez-Gross, H. A.; Dougherty, W. M.; Lin, B. Y.; Zieve, J. J.; Martinez-Garcia, P. J.; Holt, C.; Yandell, M.; Zimin, A. V.; Yorke, J. A.; Crepeau, M. W.; Puiu, D.; Salzberg, S. L.; de Jong, P. J.; Mockaitis, Keithanne; Main, Dorrie; Langley, C. H.; Neale, D. B.; Barnett, William K WK William K.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; LeDuc, RD D Richard D.; Fellers, RT; Early, BP; Greer, JB; Ganote, CL Carrie L.; Podicheti, Ram; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; McGrath, Casey L. CL; Gout, JF Jean-Francois JF; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Yanagi, Akira; Lynch, Michael; Ping, Robert J; Miller, Therese; Plale, Beth; Stewart, Craig CA A Craig A.; Ping, Robert J; Plale, Beth; Stewart, Craig CA A Craig A.; Barnett, William K WK William K.; Stewart, Craig CA A Craig A.; Miller, Therese; Blood, Philip D. Phillip D.; Tillotson, J; Froelich, W; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Ganote, CL Carrie L.; McGrath, Casey L. CL; Gout, JF Jean-Francois JF; Johri, Parul; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Brown, James B.; Boley, Nathan; Eisman, Robert; May, Gregory D. Gemma E.; Stoiber, Marcus H.; Duff, Michael O.; Booth, Ben W.; Wen, Jiayu; Park, Soo; Suzuki, Ana Maria; Wan, Kenneth H.; Yu, Charles; Zhang, Dayu; Carlson, Joseph W.; Cherbas, Lucy; Eads, Brian D.; Miller, David; Mockaitis, Keithanne; Roberts, Johnny; Davis, Carrie A.; Frise, Erwin; Hammonds, Ann S.; Olson, Sara; Shenker, Sol; Sturgill, David; Samsonova, Anastasia A.; Weiszmann, Richard; Robinson, Garret; Hernandez, Juan; Andrews, Justen; Bickel, Peter J.; Carninci, Piero; Cherbas, Peter; Gingeras, Thomas R.; Hoskins, Roger A.; Kaufman, Thomas C.; Lai, Eric C.; Oliver, Brian; Perrimon, Norbert; Graveley, Brenton R.; Celniker, Susan E.; Chen, Xiao; Bracht, JR John R; Goldman, AD Aaron D; Dolzhenko, E; LeDuc, RD D Richard D.; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Barnett, William K WK William K.; Ganote, CL Carrie L.; Kuhn, DN David N; Dillon, NL; Innes, DJ; Wu, Le-Shin S LS; Lenz, PH Petra H.; Roncalli, Vittoria; Hassett, RP; Wu, Le-Shin S LS; Cieslak, MC Matthew C MC; Ganote, CL Carrie L.; Wu, Le-Shin S LS; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; LeDuc, RD D Richard D.; Wu, Le-Shin S LS; Christie, Andrew E.; Roncalli, Vittoria; Wu, Le-Shin S LS; Ganote, CL Carrie L.; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Lenz, PH Petra H.; Swart, Estienne C; Bracht, JR John R; Magrini, Vincent; Minx, Patrick; Chen, Xiao; Zhou, Yi; Khurana, Jaspreet S; Goldman, AD Aaron D; Nowacki, Mariusz; Schotanus, Klaas; Jung, Seolkyoung; Fulton, Robert S; Ly, Amy; McGrath, Sean; Haub, Kevin; Wiggins, Jessica L; Storton, Donna; Matese, John C; Parsons, Lance; Chang, Wei-Jen Jen; Bowen, Michael S; Stover, Nicholas A; Jones, Thomas A; Eddy, Sean R; Herrick, Glenn A; Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G; Wilson, Richard K; Mardis, Elaine R; Landweber, Laura F; LeDuc, RD D Richard D.; Stewart, Craig CA A Craig A.; Barnett, William K WK William K.; Link, Matthew R.; Shankar, G; Miller, Therese; Hayashi, S; Gesing, S; Quick, R; Teige, S; Ganote, CL Carrie L.; Barnett, William K WK William K.; LeDuc, RD D Richard D.; Barnett, William K WK William K.; Wu, Le-Shin S LS; Ganote, CL Carrie L.; Doak, Thomas G. TG A},
 private_publication = {false},
 abstract = {This research is based upon work supported by the National Science Foundation under grant No. ABI-1458641 to Indiana University.},
 bibtype = {article},
 author = {Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Blood, Philip D. Phillip D. and Sanders, Sheri A. and Papudeshi, Bhavya Nalagampalli and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Mansfield, Charles and Tseng, Chi Yen and Custer, Thomas and Custer, Christine and Matson, Cole and Johri, Parul and Marinov, Georgi K and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Lynch, Michael and Cai, Jasmine X.; Weathers, Jania G.; Leffler, Haley; Ganapaneni, Sruthi; Papudeshi, Bhavya; Sanders, Sheri; Doak, Thomas G and Sanders, Sheri A. and Papudeshi, Bhavya Nalagampalli and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Chafin, Tyler and Reshetnikov, Andrey and Sokolov, Sergey and Pummil, Jeff and Douglas, Michael Marlis and Douglas, Michael Marlis and Sander, Sheri and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Leffler, Haley and Ganapaneni, Sruthi and Papudeshi, Bhavya Nalagampalli and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Cai, Jasmine X and Weathers, Jania G and Leffler, Haley and Ganapaneni, Sruthi and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Foran, Eliza G.; Suggs, Evan D.; Underwood, Tenecious A.; Snapp-Childs, Winona; Sanders, Sheri A and Foran, Eliza and Anderson, Jazzly and Slayton, Thomas and Guido, Emmanuel and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Sanders, Sheri A. and Russell, Kristin and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Papudeshi, Bhavya Nalagampalli and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Podicheti, Ram and Yang, Tianhong and Fang, Lingling and Jayanthi, Srinivas and Rajan, Gayathri and Kumar, Thallapuranam Krishnaswarmy Suresh and Medina-Bolivar, Fabricio and Mockaitis, Keithanne and Sanders, Sheri A. and Jayanthi, Srinivas and Rajan, Gayathri and Podicheti, Ram and Thallapuranam, Suresh Kumar and Mockaitis, Keithanne and Medina-Bolivar, Fabricio and Long, Hongan., Doak, G, Thomas., Lynch, Michael. and Michaels, Scott D. SD D ( and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Michaels, Scott D. SD D ( and Ganote, Carrie CL Carrie L. and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Behringer, Megan G and Choi, Brian I and Miller, Samuel F and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Karty, Jonathan A and Guo, Wanfeng and Lynch, Michael and Anderson, Jazzly and Slayton, Thomas and Guido, Emmanuel and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Mendes, Fabio and Henschel, Robert and Hahn, Matthew and Fulton, Ben and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Fischer, Jeremy and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Wernert, Julie and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Papudeshi, Bhavya Nalagampalli and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Sanders, Sheri A. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Mockaitis, Keithanne and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Hancock, David Y. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Wernert, Julie and Miller, Therese and Bhavya, Papudeshi and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Blood, Philip D. Phillip D. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Haas, Brian BJ and Dobin, Alexander and Stransky, Nicolas and Li, Bo and Yang, Xiao and Tickle, Timothy and Bankapur, Asma and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Pochet, Natalie and Sun, Jing and Wu, Catherine and Gingeras, Thomas R. and Regev, Aviv and Doak Craig A Stewart Scott D Michaels, Thomas G and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Michaels, Scott D. SD D ( and Papudeshi, Bhavya Nalagampalli and Haggerty, J. Matthew and Doane, Michael and Morris, Megan M. and Walsh, Kevin and Beattie, Douglas T. and Pande, Dnyanada and Zaeri, Parisa and Silva, Genivaldo G.Z. and Thompson, Fabiano and Edwards, Robert A. and Dinsdale, Elizabeth A. and Sanders, Sheri A. and Pfrender, Michael E and Blood, Philip D. Phillip D. and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Papudeshi, Bhavya Nalagampalli and Blood, Philip D. Phillip D. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Klegarth, A R and Sanders, Sheri A. and Gloss, A D and Lane‐deGraaf, K E and Jones‐Engel, L and Fuentes, A and Hollocher, H and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Wernert, Julie and Hancock, David Y. and Miller, Therese and Plale, Beth and Welch, Von and Pierce, Marlon and Fox, Geoffrey C. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Hancock, David Y. and Henschel, Robert and Link, Matthew R. and Miller, Therese and Wernert, Eric and Boyles, Michael J. and Fulton, Ben and Weakley, Le Mai and Ping, Robert J and Gniady, Tassie and Snapp-Childs, Winona and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Blood, Philip D. Phillip D. and Sanders, Sheri A. and Stewart, Craig CA A Craig A. and Michaels, Scott D. SD D ( and Ackerman, Matthew S and Johri, Parul and Spitze, Ken and Xu, Sen and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Young, Kimberly and Lynch, Michael and Krenek, Sascha and Marinov, Georgi K and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Berendonk, Thomas U and Lynch, Michael and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Hallock, Barb and Blood, Philip D. Phillip D. and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Brokaw, Cicada and Bhavya, N P and Haas, Brian BJ and Ganote, Carrie CL Carrie L. and Zaila, Kassandra E. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ellerbrock, Hannah and Tung, Che Huang and Martins, Mauricio L. and Kolbin, Daniel and Yao, Meng Chao and Cassidy-Hanley, Donna M. and Clark, Theodore G. and Chang, Wei-Jen Jen and Sczyrba, Alexander and Hofmann, Peter and Belmann, Peter and Koslicki, David and Janssen, Stefan and Droege, Johannes and Gregor, Ivan and Majda, Stephan and Fiedler, Jessika and Dahms, Eik and Bremges, Andreas and Fritz, Adrian and Garrido-Oter, Ruben and Jorgensen, Tue S and Shapiro, Nicole and Blood, Philip D. Phillip D. and Gurevich, Alexey and Bai, Yang and Turaev, Dmitrij and DeMaere, Matthew Z and Chikhi, Rayan and Nagarajan, Niranjan and Quince, Christopher and Hansen, Lars H and Sorensen, Soren J and Chia, Burton K H and Denis, Bertrand and Froula, Jeff L and Wang, Zhong and Egan, Robert and Kang, Dongwan D and Cook, Jeffrey J and Deltel, Charles and Beckstette, Michael and Lemaitre, Claire and Peterlongo, Pierre and Rizk, Guillaume and Lavenier, Dominique and Wu, Yu-Wei Ye and Singer, Steven W and Jain, Chirag and Strous, Marc and Klingenberg, Heiner and Meinicke, Peter and Barton, Michael and Lingner, Thomas and Lin, Hsin-Hung and Liao, Yu-Chieh and Gueiros, Genivaldo and Cuevas, Daniel A and Edwards, Robert A. and Saha, Surya and Piro, Vitor C and Renard, Bernhard Y and Pop, Mihai and Klenk, Hans-Peter and Goeker, Markus and Kyrpides, Nikos and Woyke, Tanja and Vorholt, Julia A and Schulze-Lefert, Paul and Rubin, Edward M and Darling, Aaron E and Rattei, Thomas and McHardy, Alice C and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Tydecks, Laura and Bremerich, Vanessa and Jentschke, Ilona and Likens, Gene E. and Tockner, Klement and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Blood, Philip D. Phillip D. and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ghaffari, Noushin and Abante, Jordi and Singh, Raminder and Blood, Philip D. Phillip D. and Johnson, Charles D. and Kucukyildirim, Sibel and Long, Hongan and Sung, Way and Miller, Samuel F and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Lynch, Michael and Chandran, Uma R and Medvedeva, Olga P and Barmada, M Michael and Blood, Philip D. Phillip D. and Chakka, Anish and Luthra, Soumya and Ferreira, Antonio and Wong, Kim F and Lee, Adrian V. and Zhang, Zhihui and Budden, Robert and Scott, J Ray and Berndt, Annerose and Berg, Jeremy M and Jacobson, Rebecca S and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Stewart, Craig CA A Craig A. and Michaels, Scott D. SD D ( and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Lee, Heewook and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Popodi, Ellen and Foster, Patricia L and Tang, Haixu and Sanders, Sheri A. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Blood, Philip D. Phillip D. and Ganote, Carrie CL Carrie L. and Sanders, Sheri A. and Nimkulrat, Sutichot and Lee, Heewook and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Ntai, I and LeDuc, RD D Richard D. and Fellers, RT and Neeman, Henry and Bergstrom, Aaron and Brunson, Dana and Ganote, Carrie CL Carrie L. and Gray, Zane and Guilfoos, Brian and Kalescky, Robert and Lemley, Evan and Moore, Brian G and Ramadugu, Sai Kumar and Romanella, Alana and Rush, Johnathan and Sherman, Andrew H and Stengel, Brian and Voss, Dan and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Barnett, William K WK William K. and Seetharam, Arun and Gomez, Antonio and Purcell, Catherine M and Hyde, John R and Blood, Philip D. Phillip D. and Severin, Andrew J and Uy, KL and LeDuc, RD D Richard D. and Ganote, Carrie CL Carrie L. and Wang, M and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Ganote, Carrie CL Carrie L. and Hallock, Barb and Lee, F J and Rusch, D B and Stewart, F J and Zhang, Yujia Yuehua and Kong, Weijing and Gao, Yang and Liu, Xiaoyan and Gao, Kai and Xie, Han and Wu, Yu-Wei Ye and Zhang, Yujia Yuehua and Wang, Jingmin and Gao, Feng and Wu, Xiru and Jiang, Yuwu and Youssef, N. H. and Couger, M. Brian and Struchtemeyer, C. G. and Liggenstoffer, A. S. and Prade, R. A. and Najar, F. Z. and Atiyeh, H. K. and Wilkins, M. R. and Elshahed, M. S. and Wu, Zhiqiang and Yang, Li and Ren, Xianwen and He, Guimei and Zhang, Junpeng Jin and Yang, Jian and Qian, Zhaohui and Dong, Jie and Sun, Lilian and Zhu, Yafang and Du, Jiang and Yang, Fan and Zhang, Shuyi and Jin, Qi and Uy, KL and LeDuc, RD D Richard D. and Ganote, Carrie CL Carrie L. and Tarpy, David R and Mattila, Heather R and Newton, ILG Irene L G and Subramanian, Sandeep and Chaparala, Srilakshmi and Avali, Viji and Ganapathiraju, Madhavi K. and Stanton-Geddes, John and Paape, Timothy and Epstein, Brendan and Briskine, Roman and Yoder, Jeremy and Mudge, Joann and Bharti, Arvind K. and Farmer, Andrew D. and Zhou, Peng and Denny, Roxanne and May, Gregory D. Gemma E. and Erlandson, Stephanie and Yakub, Mohammed and Sugawara, Masayuki and Sadowsky, Michael J. and Young, Nevin D. and Tiffin, Peter and Sousounis, Konstantinos and Qi, Feng and Yadav, Manisha C and Millan, Jose Luis and Toyama, Fubito and Chiba, Chikafumi and Eguchi, Yukiko and Eguchi, Goro and Tsonis, Panagiotis A and Roncalli, Vittoria and Cieslak, MC Matthew C MC and Lenz, PH Petra H. and Rokop, Z P and Horton, Melissa A and Newton, ILG Irene L G and Raborn, RT Taylor and Spitze, Ken and Brendel, Volker P VP and Lynch, Michael and Qin, Xiaomei and Huang, Sheng and Liu, Yanqing and Bian, Mingdi and Shi, Wuliang and Zuo, Zecheng and Yang, Zhenming and Pipes, Lenore and Li, Sheng and Bozinoski, Marjan and Palermo, Robert E. and Peng, Xinxia and Blood, Philip D. Phillip D. and Kelly, Sara and Weiss, Jeffrey M. and Thierry-Mieg, Jean and Thierry-Mieg, Danielle and Zumbo, Paul and Chen, Ronghua and Schroth, Gary P. and Mason, Christopher E. and Katze, Michael G. and Phuong, Mark Anthony and Mahardika, Gusti N and Peterson, M and Malloy, J and Buonaccorsi, V and Marden, J and Petersen, Isaac T. and Bates, John E. and Dodge, Kenneth A. and Lansford, Jennifer E. and Pettit, Gregory S. and Peng, Xinxia and Pipes, Lenore and Xiong, Hao and Green, Richard R. and Jones, Daniel C. and Ruzzo, Walter L. and Schroth, Gary P. and Mason, Christopher E. and Palermo, Robert E. and Katze, Michael G. and Orsini, Luisa and Gilbert, Donald and Podicheti, Ram and Jansen, Mieke and Brown, James B. and Solari, Omid Shams and Spanier, Katina I and Colbourne, John K and Rush, Douglas and Decaestecker, Ellen and Asselman, Jana and De Schamphelaere, Karel A C and Ebert, Dieter and Haag, Christoph R and Kvist, Jouni and Laforsch, Christian and Petrusek, Adam and Beckerman, Andrew P and Little, Tom J and Chaturvedi, Anurag and Pfrender, Michael E and De Meester, Luc and Frilander, Mikko J and Newton, ILG Irene L G and Sheehan, KB Kathy B and Motamayor, Juan C and Mockaitis, Keithanne and Schmutz, Jeremy and Haiminen, Niina and III, Donald Livingstone and Cornejo, Omar and Findley, Seth D and Zheng, Ping and Utro, Filippo and Royaert, Stefan and Saski, Christopher and Jenkins, Jerry and Podicheti, Ram and Zhao, Meixia and Scheffler, Brian E and Stack, Joseph C and Feltus, Frank A and Mustiga, Guiliana M and Amores, Freddy and Phillips, Wilbert and Marelli, Jean Philippe and May, Gregory D. Gemma E. and Shapiro, Howard and Ma, Jianxin and Bustamante, Carlos D and Schnell, Raymond J and Main, Dorrie and Gilbert, Donald and Parida, Laxmi and Kuhn, DN David N and McGrath, Casey L. CL and Gout, JF Jean-Francois JF and Johri, Parul and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Yanagi, Akira and Lynch, Michael and Martínez, Teresa and Ropelewski, Alexander J and González-Mendez, Ricardo and Vázquez, Guillermo J and Robledo, Iraida E. and Martinez, Teresa and Aquino, Edna E. and Robledo, Iraida E. and Martinez, Idali and Vazquez, Guillermo J. and Aquino, Edna E. and Robledo, Iraida E. and Lipovich, Leonard and Hou, Zhuo-Cheng and Jia, Hui and Sinkler, Christopher and McGowen, Michael and Sterner, Kirstin N. and Weckle, Amy and Sugalski, Amara B. and Pipes, Lenore and Gatti, Domenico L. and Mason, Christopher E. and Sherwood, Chet C. and Hof, Patrick R. and Kuzawa, Christopher W. and Grossman, Lawrence I. and Goodman, Morris and Wildman, Derek E. and Kuhn, DN David N and Dillon, NL and Innes, DJ and Wu, Le-Shin S LS and Krishnakumar, Raga and Chen, Amy F and Pantovich, Marisol G and Danial, Muhammad and Parchem, Ronald J and Labosky, Patricia A and Blelloch, Robert and Jin, M and Bothfeld, W and Austin, S and Sato, TK and Reau, A La and Huth, Troy J and Place, Sean P and Horton, Melissa A and Oliver, Randy and Newton, ILG Irene L G and Gulia-Nuss, Monika and Nuss, Andrew B and Meyer, Jason M and Sonenshine, Daniel E and Roe, R Michael and Waterhouse, Robert M and Sattelle, David B and de la Fuente, Jose and Ribeiro, Jose M and Megy, Karine and Thimmapuram, Jyothi and Miller, Jason R and Walenz, Brian P and Koren, Sergey and Hostetler, Jessica B and Thiagarajan, Mathangi and Joardar, Vinita S and Hannick, Linda I and Bidwell, Shelby and Hammond, Martin P and Young, Sarah and Zeng, Qiandong and Abrudan, Jenica L and Almeida, Francisca C and Ayllon, Nieves and Bhide, Ketaki and Bissinger, Brooke W and Bonzon-Kulichenko, Elena and Buckingham, Steven D and Caffrey, Daniel R and Caimano, Melissa J and Croset, Vincent and Driscoll, Timothy and Gilbert, Donald and Gillespie, Joseph J and Giraldo-Calderon, Gloria I and Grabowski, Jeffrey M and Jiang, David and Khalil, Sayed M S and Kim, Donghun and Kocan, Katherine M and Koci, Juraj and Kuhn, Richard J and Kurtti, Timothy J and Lees, Kristin and Lang, Emma G and Kennedy, Ryan C and Kwon, Hyeogsun and Perera, Rushika and Qi, Yumin and Radolf, Justin D and Sakamoto, Joyce M and Sanchez-Gracia, Alejandro and Severo, Maiara S and Silverman, Neal and Simo, Ladislav and Tojo, Marta and Tornador, Cristian and Van Zee, Janice P and Vazquez, Jesus and Vieira, Filipe G and Villar, Margarita and Wespiser, Adam R and Yang, Yunlong and Zhu, Jiwei and Arensburger, Peter and Pietrantonio, Patricia V and Barker, Stephen C and Shao, Renfu and Zdobnov, Evgeny M and Hauser, Frank and Grimmelikhuijzen, Cornelis J P and Park, Yoonseong and Rozas, Julio and Benton, Richard and Pedra, Joao H F and Nelson, David R and Unger, Maria F and Tubio, Jose M C and Tu, Zhijian and Robertson, Hugh M and Shumway, Martin and Sutton, Granger and Wortman, Jennifer R and Lawson, Daniel and Wikel, Stephen K and Nene, Vishvanath M and Fraser, Claire M and Collins, Frank H and Birren, Bruce and Nelson, Karen E and Caler, Elisabet and Hill, Catherine A and Ghaffari, Noushin and Sanchez-Flores, Alejandro and Doan, Ryan and Garcia-Orozco, Karina D. and Chen, Patricia L. and Ochoa-Leyva, Adrian and Lopez-Zavala, Alonso A. and Carrasco, J. Salvador and Hong, Chris and Brieba, Luis G. and Rudiño-Piñera, Enrique and Blood, Philip D. Phillip D. and Sawyer, Jason E. and Johnson, Charles D. and Dindot, Scott V. and Sotelo-Mundo, Rogerio R. and Criscitiello, Michael F. and Gao, Kai and Tankovic, Anel and Zhang, Yujia Yuehua and Kusumoto, Hirofumi and Zhang, Junpeng Jin and Chen, Wenjuan and XiangWei, Wenshu and Shaulsky, Gil H. and Hu, Chun and Traynelis, Stephen F. and Yuan, Hongjie and Jiang, Yuwu and Fergus, Daniel J and Feng, Ni Y and Bass, Andrew H and Fergus, Daniel J and Bass, Andrew H and Duncan, Rebecca P and Feng, Honglin and Nguyen, Douglas M and Wilson, Alex C C and Darris, Carl E and Tyus, James E and Kelley, Gary and Ropelewski, Alexander J and Nicholas, Hugh B and Wang, Xiaofei and Nahashon, Samuel and Nahashon, Samuel and Couger, M. Brian and Pipes, Lenore and Squina, F and Boyd, Bret M. and Allen, Julie M. and Nguyen, Nam and Sweet, Andrew D. and Warnow, Tandy and Shapiro, Michael D. and Villa, Scott M. and Bush, Sarah E. and Clayton, Dale H. and Johnson, Kevin P. and Blood, Philip D. Phillip D. and Marcus, Shoshana and Schatz, Michael C. and Bahreini, Amir and Levine, Kevin and Santana-Santos, Lucas and Benos, Panayiotis V. and Wang, Peilu and Andersen, Courtney and Oesterreich, Steffi and Lee, Adrian V. and Armstrong, Eric J. and Stillman, Jonathon H. and Arafat, Ahmed and Jing, Peng and Ma, Yuping and Pu, Miao and Nan, Gai and Fang, He and Chen, Chen and Fei, Yin and Almada, Amalia A. and Tarrant, Ann M. and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Bao, G and Wang, M and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Barnett, William K WK William K. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Wu, Le-Shin S LS and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and LeDuc, RD D Richard D. and Vaughn, Matthew and Fonner, JM and Zhang, Quan and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Hallock, Barb and Ganote, Carrie CL Carrie L. and Pespeni, M and Hayashi, S and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Barnett, William K WK William K. and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Wegrzyn, J. L. and Liechty, J. D. and Stevens, K. A. and Wu, Le-Shin S LS and Loopstra, C. A. and Vasquez-Gross, H. A. and Dougherty, W. M. and Lin, B. Y. and Zieve, J. J. and Martinez-Garcia, P. J. and Holt, C. and Yandell, M. and Zimin, A. V. and Yorke, J. A. and Crepeau, M. W. and Puiu, D. and Salzberg, S. L. and de Jong, P. J. and Mockaitis, Keithanne and Main, Dorrie and Langley, C. H. and Neale, D. B. and Barnett, William K WK William K. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and LeDuc, RD D Richard D. and Fellers, RT and Early, BP and Greer, JB and Ganote, Carrie CL Carrie L. and Podicheti, Ram and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and McGrath, Casey L. CL and Gout, JF Jean-Francois JF and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Yanagi, Akira and Lynch, Michael and Ping, Robert J and Miller, Therese and Plale, Beth and Stewart, Craig CA A Craig A. and Ping, Robert J and Plale, Beth and Stewart, Craig CA A Craig A. and Barnett, William K WK William K. and Stewart, Craig CA A Craig A. and Miller, Therese and Blood, Philip D. Phillip D. and Tillotson, J and Froelich, W and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ganote, Carrie CL Carrie L. and McGrath, Casey L. CL and Gout, JF Jean-Francois JF and Johri, Parul and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Brown, James B. and Boley, Nathan and Eisman, Robert and May, Gregory D. Gemma E. and Stoiber, Marcus H. and Duff, Michael O. and Booth, Ben W. and Wen, Jiayu and Park, Soo and Suzuki, Ana Maria and Wan, Kenneth H. and Yu, Charles and Zhang, Dayu and Carlson, Joseph W. and Cherbas, Lucy and Eads, Brian D. and Miller, David and Mockaitis, Keithanne and Roberts, Johnny and Davis, Carrie A. and Frise, Erwin and Hammonds, Ann S. and Olson, Sara and Shenker, Sol and Sturgill, David and Samsonova, Anastasia A. and Weiszmann, Richard and Robinson, Garret and Hernandez, Juan and Andrews, Justen and Bickel, Peter J. and Carninci, Piero and Cherbas, Peter and Gingeras, Thomas R. and Hoskins, Roger A. and Kaufman, Thomas C. and Lai, Eric C. and Oliver, Brian and Perrimon, Norbert and Graveley, Brenton R. and Celniker, Susan E. and Chen, Xiao and Bracht, JR John R and Goldman, AD Aaron D and Dolzhenko, E and LeDuc, RD D Richard D. and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Barnett, William K WK William K. and Ganote, Carrie CL Carrie L. and Kuhn, DN David N and Dillon, NL and Innes, DJ and Wu, Le-Shin S LS and Lenz, PH Petra H. and Roncalli, Vittoria and Hassett, RP and Wu, Le-Shin S LS and Cieslak, MC Matthew C MC and Ganote, Carrie CL Carrie L. and Wu, Le-Shin S LS and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and LeDuc, RD D Richard D. and Wu, Le-Shin S LS and Christie, Andrew E. and Roncalli, Vittoria and Wu, Le-Shin S LS and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Lenz, PH Petra H. and Swart, Estienne C and Bracht, JR John R and Magrini, Vincent and Minx, Patrick and Chen, Xiao and Zhou, Yi and Khurana, Jaspreet S and Goldman, AD Aaron D and Nowacki, Mariusz and Schotanus, Klaas and Jung, Seolkyoung and Fulton, Robert S and Ly, Amy and McGrath, Sean and Haub, Kevin and Wiggins, Jessica L and Storton, Donna and Matese, John C and Parsons, Lance and Chang, Wei-Jen Jen and Bowen, Michael S and Stover, Nicholas A and Jones, Thomas A and Eddy, Sean R and Herrick, Glenn A and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Wilson, Richard K and Mardis, Elaine R and Landweber, Laura F and LeDuc, RD D Richard D. and Stewart, Craig CA A Craig A. and Barnett, William K WK William K. and Link, Matthew R. and Shankar, G and Miller, Therese and Hayashi, S and Gesing, S and Quick, R and Teige, S and Ganote, Carrie CL Carrie L. and Barnett, William K WK William K. and LeDuc, RD D Richard D. and Barnett, William K WK William K. and Wu, Le-Shin S LS and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Blood, Philip D. Phillip D. and Vaughn, Matthew and Boscaro, Vittorio and Felletti, Michele and Vannini, Claudia and Ackerman, Matthew S and Chain, Patrick S G and Malfatti, Stephanie and Vergez, Lisa M and Shin, Maria and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Lynch, Michael and Petroni, Giulio and Haas, Brian BJ and Papanicolaou, A and Yassour, M and Grabherr, M and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Barnett, William K WK William K. and LeDuc, RD D Richard D. and Ganote, Carrie CL Carrie L. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Barnett, William K WK William K. and LeDuc, RD D Richard D. and Rho, Mina and Wu, Yu-Wei Ye and Tang, Haixu and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Rho, Mina and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ye, Yuzhen and Barnett, William K WK William K. and LeDuc, RD D Richard D. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Wu, Le-Shin S LS and Stewart, Craig CA A Craig A. and Henschel, Robert and Barnett, William K WK William K. and Shankar, G and Hancock, David Y. and Allen, M and Bolte, J and Wernert, Julie and Seiffert, K and Simms, S C and Link, Matthew R. and LeDuc, RD D Richard D. and Barnett, William K WK William K. and LeDuc, RD D Richard D. and Henschel, Robert and Lieber, M and Wu, Le-Shin S LS and Nista, PM and LeDuc, RD D Richard D. and Stewart, Craig CA A Craig A. and Henschel, Robert and Barnett, William K WK William K. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G and Ganapaneni, Sruthi and Leffler, Haley and Papudeshi, Bhavya Nalagampalli and Sanders, Sheri A. and Doak, Thomas G. TG A TG Thomas G. T.G. Tom G TG Thomas G TG Thomas G},
 editor = {Guttman, David S.},
 journal = {Mount Desert Island Biological Laboratory},
 number = {1}
}

@article{greco_scr7_2016,
	title = {{SCR7} is neither a selective nor a potent inhibitor of human {DNA} ligase {IV}},
	volume = {43},
	issn = {1568-7856},
	doi = {10.1016/j.dnarep.2016.04.004},
	abstract = {DNA ligases are attractive therapeutics because of their involvement in completing the repair of almost all types of DNA damage. A series of DNA ligase inhibitors with differing selectivity for the three human DNA ligases were identified using a structure-based approach with one of these inhibitors being used to inhibit abnormal DNA ligase IIIα-dependent repair of DNA double-strand breaks (DSB)s in breast cancer, neuroblastoma and leukemia cell lines. Raghavan and colleagues reported the characterization of a derivative of one of the previously identified DNA ligase inhibitors, which they called SCR7 (designated SCR7-R in our experiments using SCR7). SCR7 appeared to show increased selectivity for DNA ligase IV, inhibit the repair of DSBs by the DNA ligase IV-dependent non-homologous end-joining (NHEJ) pathway, reduce tumor growth, and increase the efficacy of DSB-inducing therapeutic modalities in mouse xenografts. In attempting to synthesize SCR7, we encountered problems with the synthesis procedures and discovered discrepancies in its reported structure. We determined the structure of a sample of SCR7 and a related compound, SCR7-G, that is the major product generated by the published synthesis procedure for SCR7. We also found that SCR7-G has the same structure as the compound (SCR7-X) available from a commercial vendor (XcessBio). The various SCR7 preparations had similar activity in DNA ligation assay assays, exhibiting greater activity against DNA ligases I and III than DNA ligase IV. Furthermore, SCR7-R failed to inhibit DNA ligase IV-dependent V(D)J recombination in a cell-based assay. Based on our results, we conclude that SCR7 and the SCR7 derivatives are neither selective nor potent inhibitors of DNA ligase IV.},
	language = {eng},
	journal = {DNA repair},
	author = {Greco, George E. and Matsumoto, Yoshihiro and Brooks, Rhys C. and Lu, Zhengfei and Lieber, Michael R. and Tomkinson, Alan E.},
	year = {2016},
	pmid = {27235626},
	pmcid = {PMC5042453},
	keywords = {Animals, Antineoplastic Agents, Cell Line, Tumor, Cell Survival, DNA, DNA Breaks, Double-Stranded, DNA End-Joining Repair, DNA Ligase ATP, DNA double strand break repair, DNA ligase inhibitors, Enzyme Inhibitors, Epithelial Cells, Escherichia coli, Gene Expression, Human DNA ligases, Humans, Leukocytes, Mice, Neurons, Non-homologous end-joining, Pyrimidines, Recombinant Proteins, Schiff Bases, Substrate Specificity, Tumor Burden, V(D)J Recombination, Xenograft Model Antitumor Assays},
	pages = {18--23},
}

@article{arno_mutations_2016,
	title = {Mutations in {REEP6} {Cause} {Autosomal}-{Recessive} {Retinitis} {Pigmentosa}},
	volume = {99},
	issn = {1537-6605},
	doi = {10.1016/j.ajhg.2016.10.008},
	abstract = {Retinitis pigmentosa (RP) is the most frequent form of inherited retinal dystrophy. RP is genetically heterogeneous and the genes identified to date encode proteins involved in a wide range of functional pathways, including photoreceptor development, phototransduction, the retinoid cycle, cilia, and outer segment development. Here we report the identification of biallelic mutations in Receptor Expression Enhancer Protein 6 (REEP6) in seven individuals with autosomal-recessive RP from five unrelated families. REEP6 is a member of the REEP/Yop1 family of proteins that influence the structure of the endoplasmic reticulum but is relatively unstudied. The six variants identified include three frameshift variants, two missense variants, and a genomic rearrangement that disrupts exon 1. Human 3D organoid optic cups were used to investigate REEP6 expression and confirmed the expression of a retina-specific isoform REEP6.1, which is specifically affected by one of the frameshift mutations. Expression of the two missense variants (c.383C{\textgreater}T [p.Pro128Leu] and c.404T{\textgreater}C [p.Leu135Pro]) and the REEP6.1 frameshift mutant in cultured cells suggest that these changes destabilize the protein. Furthermore, CRISPR-Cas9-mediated gene editing was used to produce Reep6 knock-in mice with the p.Leu135Pro RP-associated variant identified in one RP-affected individual. The homozygous knock-in mice mimic the clinical phenotypes of RP, including progressive photoreceptor degeneration and dysfunction of the rod photoreceptors. Therefore, our study implicates REEP6 in retinal homeostasis and highlights a pathway previously uncharacterized in retinal dystrophy.},
	language = {eng},
	number = {6},
	journal = {American Journal of Human Genetics},
	author = {Arno, Gavin and Agrawal, Smriti A. and Eblimit, Aiden and Bellingham, James and Xu, Mingchu and Wang, Feng and Chakarova, Christina and Parfitt, David A. and Lane, Amelia and Burgoyne, Thomas and Hull, Sarah and Carss, Keren J. and Fiorentino, Alessia and Hayes, Matthew J. and Munro, Peter M. and Nicols, Ralph and Pontikos, Nikolas and Holder, Graham E. and {UKIRDC} and Asomugha, Chinwe and Raymond, F. Lucy and Moore, Anthony T. and Plagnol, Vincent and Michaelides, Michel and Hardcastle, Alison J. and Li, Yumei and Cukras, Catherine and Webster, Andrew R. and Cheetham, Michael E. and Chen, Rui},
	month = dec,
	year = {2016},
	pmid = {27889058},
	pmcid = {PMC5142109},
	keywords = {Adolescent, Alleles, Animals, Child, Child, Preschool, Eye Proteins, Female, Genes, Recessive, Humans, Induced Pluripotent Stem Cells, Male, Membrane Transport Proteins, Mice, Mutation, Mutation, Missense, Phenotype, Photoreceptor Cells, Vertebrate, Retinitis Pigmentosa, Young Adult},
	pages = {1305--1315}
}

Paper  doi  abstract   bibtex   1 download  

@article{felten_vibrational_2015,
	title = {Vibrational spectroscopic image analysis of biological material using multivariate curve resolution-alternating least squares ({MCR}-{ALS})},
	volume = {10},
	issn = {1750-2799 (Electronic) 1750-2799 (Linking)},
	url = {https://www.ncbi.nlm.nih.gov/pubmed/25569330},
	doi = {10.1038/nprot.2015.008},
	abstract = {Raman and Fourier transform IR (FTIR) microspectroscopic images of biological material (tissue sections) contain detailed information about their chemical composition. The challenge lies in identifying changes in chemical composition, as well as locating and assigning these changes to different conditions (pathology, anatomy, environmental or genetic factors). Multivariate data analysis techniques are ideal for decrypting such information from the data. This protocol provides a user-friendly pipeline and graphical user interface (GUI) for data pre-processing and unmixing of pixel spectra into their contributing pure components by multivariate curve resolution-alternating least squares (MCR-ALS) analysis. The analysis considers the full spectral profile in order to identify the chemical compounds and to visualize their distribution across the sample to categorize chemically distinct areas. Results are rapidly achieved (usually {\textless}30-60 min per image), and they are easy to interpret and evaluate both in terms of chemistry and biology, making the method generally more powerful than principal component analysis (PCA) or heat maps of single-band intensities. In addition, chemical and biological evaluation of the results by means of reference matching and segmentation maps (based on k-means clustering) is possible.},
	language = {en},
	number = {2},
	urldate = {2021-06-07},
	journal = {Nat Protoc},
	author = {Felten, J. and Hall, H. and Jaumot, J. and Tauler, R. and de Juan, A. and Gorzsas, A.},
	month = feb,
	year = {2015},
	note = {Edition: 2015/01/09},
	keywords = {*Multivariate Analysis, *Spectroscopy, Fourier Transform Infrared, *Spectrum Analysis, Raman, Animals, Image Processing, Computer-Assisted/*methods, Islets of Langerhans/chemistry, Least-Squares Analysis, Mice, Inbred C57BL, Populus/chemistry, User-Computer Interface, Xylem/chemistry},
	pages = {217--40},
}

@article{motenko_mousemine:_2015,
	title = {{MouseMine}: a new data warehouse for {MGI}},
	volume = {26},
	issn = {1432-1777},
	shorttitle = {{MouseMine}},
	doi = {10.1007/s00335-015-9573-z},
	abstract = {MouseMine (www.mousemine.org) is a new data warehouse for accessing mouse data from Mouse Genome Informatics (MGI). Based on the InterMine software framework, MouseMine supports powerful query, reporting, and analysis capabilities, the ability to save and combine results from different queries, easy integration into larger workflows, and a comprehensive Web Services layer. Through MouseMine, users can access a significant portion of MGI data in new and useful ways. Importantly, MouseMine is also a member of a growing community of online data resources based on InterMine, including those established by other model organism databases. Adopting common interfaces and collaborating on data representation standards are critical to fostering cross-species data analysis. This paper presents a general introduction to MouseMine, presents examples of its use, and discusses the potential for further integration into the MGI interface.},
	language = {eng},
	number = {7-8},
	journal = {Mammalian Genome: Official Journal of the International Mammalian Genome Society},
	author = {Motenko, H. and Neuhauser, S. B. and O'Keefe, M. and Richardson, J. E.},
	month = aug,
	year = {2015},
	pmid = {26092688},
	pmcid = {PMC4534495},
	keywords = {Animals, Data Mining, Databases, Genetic, Genomics, Internet, Mice, Software},
	pages = {325--330}
}

Paper  doi  abstract   bibtex   

@article{Heiker-2014-ID6,
  title     = {Identification of genetic loci associated with different responses to
               high-fat diet-induced obesity in C57{BL}/6N and C57{BL}/6J substrains.},
  abstract  = {We have recently demonstrated that C57{BL}/6{NT}ac and C57{BL}/6{JR}j
               substrains are significantly different in their response to high-fat
               diet-induced obesity ({DIO}). The C57{BL}/6{JR}j substrain seems to be
               protected from {DIO} and genetic differences between C57{BL}/6J and
               C57{BL}/6N substrains at 11 single nucleotide polymorphism ({SNP}) loci
               have been identified. To define genetic variants as well as differences in
               parameters of glucose homeostasis and insulin sensitivity between
               C57{BL}/6{NT}ac and C57{BL}/6{JR}j substrains that may explain the
               different response to {DIO}, we analyzed 208 first backcross ({BC}1)
               hybrids of C57{BL}/6{NT}ac and C57{BL}/6{JR}j [(C57{BL}/6{NT}ac ×
               C57{BL}/6{JR}j)F1 × C57{BL}/6{NT}ac] mice. Body weight, epigonadal and
               subcutaneous fat mass, circulating leptin, as well as parameters of glucose
               metabolism were measured after 10 wk of high-fat diet ({HFD}). Genetic
               profiling of {BC}1 hybrids were performed using TaqMan {SNP} genotyping
               assays. Furthermore, to assess whether {SNP} polymorphisms could affect
               m{RNA} level, we carried out gene expression analysis in murine liver
               samples. Human subcutaneous adipose tissue was used to verify murine data
               of {SNAP}29. We identified four sex-specific variants that are associated
               with the extent of {HFD}-induced weight gain and fat depot mass. {BC}1
               hybrids carrying the combination of risk or beneficial alleles exhibit the
               phenotypical extremes of the parental strains. Murine and human {SC}
               expression analysis revealed Snap29 as strongest candidate. Our data
               indicate an important role of these loci in responsiveness to {HFD}-induced
               obesity and suggest genes of the synaptic vesicle release system such as
               Snap29 being involved in the regulation of high-fat {DIO}.},
  author    = {Heiker, John T and Kunath, Anne and Kosacka, Joanna and Flehmig, Gesine and
               Knigge, Anja and Kern, Matthias and Stumvoll, Michael and Kovacs, Peter and
               Blüher, Matthias and Klöting, Nora},
  volume    = {46},
  number    = {11},
  pages     = {377--84},
  year      = {2014},
  month     = {6},
  url       = {http://www.pubmed.org/24692188},
  pmid      = {24692188},
  doi       = {10.1152/physiolgenomics.00014.2014},
  keywords  = {Animals, Humans, Mice, Male, Adipose Tissue, Alleles, Body Weight, Diet,
               High-Fat, Female, Genetic Loci, Genotype, Glucose, Leptin, Mice, Inbred
               C57{BL}, Middle Aged, Obesity, Polymorphism, Single Nucleotide, Vesicular
               Transport Proteins, Weight Gain},
  file      = {FULLTEXT:pdfs/000/000/000000006.pdf:PDF}
}

@article{kim_anisi_2014,
	title = {Anisi stellati fructus extract attenuates the in vitro and in vivo metastatic and angiogenic potential of malignant cancer cells by downregulating proteolytic activity and pro-angiogenic factors},
	volume = {45},
	issn = {1791-2423},
	doi = {10.3892/ijo.2014.2606},
	abstract = {Anisi stellati fructus (ASF), commonly known as star anise, has long been used as a traditional Chinese medicine to treat inflammation, nervousness, insomnia and pain. In recent studies, it has been demonstrated that ASF possesses anti-bacterial, anti-fungal and anti-oxidant activities, as well as exhibits inhibitory effects on capillary‑like tube formation in human umbilical vein endothelial cells (HUVECs). However, the effects of ASF extract on the metastatic potential of malignant tumor cells have not been examined. In this study, we found that daily oral administration of ASF (50 mg/kg) remarkably reduced the number of pulmonary metastatic colonies of B16F10 cells in C57BL/6J mice with no observed systemic toxicity. In an in vitro system, ASF inhibited metastatic properties, including anchorage‑independent colony formation, migration and invasion. Upon phorbol 12-myristate 13-acetate (PMA) stimulation, the mRNA levels of matrix metalloproteinases (MMPs) -9, -13, -14 and urokinase plasminogen activator (uPA) decreased in a dose-dependent manner with ASF treatment. Gelatinase, type I collagenase, and uPA activities were also suppressed efficiently by ASF treatment. In response to PMA, NF-κB and AP-1 activation as well as p38 phosphorylation, which are crucial for MMP activation, were significantly decreased by ASF. In particular, ASF considerably inhibited tumor-induced HUVEC migration and tube formation and suppressed in vivo tumor-induced angiogenesis via a reduction of pro-angiogenic factors in tumors. These results collectively indicate that ASF might be useful in the management of metastatic malignant tumors.},
	language = {eng},
	number = {5},
	journal = {International Journal of Oncology},
	author = {Kim, Aeyung and Im, Minju and Ma, Jin Yeul},
	month = nov,
	year = {2014},
	pmid = {25176510},
	keywords = {Angiogenesis Inhibitors, Animals, Cell Proliferation, Chai, Human Umbilical Vein Endothelial Cells, Illicium, Medicine, Chinese Traditional, Mice, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Plant Extracts, melanoma, metastasis, star anise},
	pages = {1937--1948},
}

@article{kalderimis_intermine:_2014,
	title = {{InterMine}: extensive web services for modern biology},
	volume = {42},
	issn = {1362-4962},
	shorttitle = {{InterMine}},
	doi = {10.1093/nar/gku301},
	abstract = {InterMine (www.intermine.org) is a biological data warehousing system providing extensive automatically generated and configurable RESTful web services that underpin the web interface and can be re-used in many other applications: to find and filter data; export it in a flexible and structured way; to upload, use, manipulate and analyze lists; to provide services for flexible retrieval of sequence segments, and for other statistical and analysis tools. Here we describe these features and discuss how they can be used separately or in combinations to support integrative and comparative analysis.},
	language = {eng},
	number = {Web Server issue},
	journal = {Nucleic Acids Research},
	author = {Kalderimis, Alex and Lyne, Rachel and Butano, Daniela and Contrino, Sergio and Lyne, Mike and Heimbach, Joshua and Hu, Fengyuan and Smith, Richard and Stěpán, Radek and Sullivan, Julie and Micklem, Gos},
	month = jul,
	year = {2014},
	pmid = {24753429},
	pmcid = {PMC4086141},
	keywords = {Animals, Chromosomes, Databases, Factual, Humans, Internet, Mice, Sequence Analysis, DNA, Software, User-Computer Interface},
	pages = {W468--472}
}

Paper  doi  abstract   bibtex   

@article{kim_chronic_2014,
	title = {Chronic exposure to ethanol of male mice before mating produces attention deficit hyperactivity disorder-like phenotype along with epigenetic dysregulation of dopamine transporter expression in mouse offspring.},
	volume = {92},
	issn = {1097-4547},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/24510599},
	doi = {10.1002/jnr.23275},
	abstract = {Preconception exposure to EtOH through the paternal route may affect neurobehavioral and developmental features of offspring. This study investigates the effects of paternal exposure to EtOH before conception on the hyperactivity, inattention, and impulsivity behavior of male offspring in mice. Sire mice were treated with EtOH in a concentration range approximating human binge drinking (0-4 g/kg/day EtOH) for 7 weeks and mated with untreated females mice to produce offspring. EtOH exposure to sire mice induced attention deficit hyperactivity disorder (ADHD)-like hyperactive, inattentive, and impulsive behaviors in offspring. As a mechanistic link, both protein and mRNA expression of dopamine transporter (DAT), a key determinant of ADHD-like phenotypes in experimental animals and humans, were significantly decreased by paternal EtOH exposure in cerebral cortex and striatum of offspring mice along with increased methylation of a CpG region of the DAT gene promoter. The increase in methylation of DAT gene promoter was also observed in the sperm of sire mice, suggesting germline changes in the epigenetic methylation signature of DAT gene by EtOH exposure. In addition, the expression of two key regulators of methylation-dependent epigenetic regulation of functional gene expression, namely, MeCP2 and DNMT1, was markedly decreased in offspring cortex and striatum sired by EtOH-exposed mice. These results suggest that preconceptional exposure to EtOH through the paternal route induces behavioral changes in offspring, possibly via epigenetic changes in gene expression, which is essential for the regulation of ADHD-like behaviors.},
	number = {5},
	urldate = {2015-05-16},
	journal = {Journal of neuroscience research},
	author = {Kim, Pitna and Choi, Chang Soon and Park, Jin Hee and Joo, So Hyun and Kim, Soo Young and Ko, Hyun Myung and Kim, Ki Chan and Jeon, Se Jin and Park, Seung Hwa and Han, Seol-Heui and Ryu, Jong Hoon and Cheong, Jae Hoon and Han, Jung Yeol and Ko, Ki Narm and Shin, Chan Young},
	month = may,
	year = {2014},
	pmid = {24510599},
	keywords = {Animals, Attention Deficit Disorder with Hyperactivity, Attention Deficit Disorder with Hyperactivity: che, Avoidance Learning, Avoidance Learning: physiology, Central Nervous System Depressants, Central Nervous System Depressants: toxicity, Disease Models, Animal, Dopamine Plasma Membrane Transport Proteins, Dopamine Plasma Membrane Transport Proteins: genet, Dopamine Plasma Membrane Transport Proteins: metab, Drinking Behavior, Epigenesis, Genetic, Epigenesis, Genetic: drug effects, Ethanol, Ethanol: toxicity, Exploratory Behavior, Exploratory Behavior: physiology, Female, Gene Expression Regulation, Gene Expression Regulation: drug effects, Male, Maze Learning, Maze Learning: physiology, Methyl-CpG-Binding Protein 2, Methyl-CpG-Binding Protein 2: genetics, Methyl-CpG-Binding Protein 2: metabolism, Mice, Mice, Inbred ICR, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, Prenatal Exposure Delayed Effects: chemically indu, Prenatal Exposure Delayed Effects: physiopathology},
	pages = {658--70},
}

@article{moverare-skrtic_osteoblast-derived_2014,
	title = {Osteoblast-derived {WNT16} represses osteoclastogenesis and prevents cortical bone fragility fractures},
	volume = {20},
	issn = {1546-170X},
	doi = {10.1038/nm.3654},
	abstract = {The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need.},
	language = {eng},
	number = {11},
	journal = {Nature Medicine},
	author = {Movérare-Skrtic, Sofia and Henning, Petra and Liu, Xianwen and Nagano, Kenichi and Saito, Hiroaki and Börjesson, Anna E. and Sjögren, Klara and Windahl, Sara H. and Farman, Helen and Kindlund, Bert and Engdahl, Cecilia and Koskela, Antti and Zhang, Fu-Ping and Eriksson, Emma E. and Zaman, Farasat and Hammarstedt, Ann and Isaksson, Hanna and Bally, Marta and Kassem, Ali and Lindholm, Catharina and Sandberg, Olof and Aspenberg, Per and Sävendahl, Lars and Feng, Jian Q. and Tuckermann, Jan and Tuukkanen, Juha and Poutanen, Matti and Baron, Roland and Lerner, Ulf H. and Gori, Francesca and Ohlsson, Claes},
	month = nov,
	year = {2014},
	pmid = {25306233},
	pmcid = {PMC4392888},
	keywords = {Aging, Animals, Cell Differentiation, Cell Line, Cell Lineage, Cells, Cultured, Disease Susceptibility, Fractures, Bone, Gene Deletion, Gene Expression Regulation, Humans, Mice, Inbred C57BL, Organ Size, Osteoblasts, Osteoclasts, Osteocytes, Osteogenesis, Osteoprotegerin, RANK Ligand, RNA, Messenger, Signal Transduction, Skull, Wnt Proteins},
	pages = {1279--1288},
}

Paper  doi  abstract   bibtex   

@article{li_regular_2013,
	title = {Regular treadmill running improves spatial learning and memory performance in young mice through increased hippocampal neurogenesis and decreased stress.},
	volume = {1531},
	issn = {1872-6240},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/23916669},
	doi = {10.1016/j.brainres.2013.07.041},
	abstract = {A substantial amount of evidence has shown that treadmill running enhances neurogenesis, improves cognitive function, and protects the brain against neurodegenerative disorders. However, treadmill running is a type of forced exercise that could increase the level of corticosterone, which subsequently down-regulates neurogenesis and impairs cognitive function. The purpose of this study was to investigate if regular treadmill running provides a balance between the positive and negative effects of treadmill running. The mice were divided into four groups: controls (CON), regular runners (RR), irregular duration runners (IDR) and irregular time-of-day runners (ITR). The RR mice ran daily on the treadmill at the same time-of-day, speed and duration. The IDR mice ran at the same time-of-day and speed, but for a different duration. The ITR mice ran at the same speed and duration, but at different time-of-day. The results showed that regular treadmill running could increase neurogenesis and improve spatial learning and memory performance, as well as decrease the level of corticosterone. The present finding emphasizes the importance of regular physical exercise on cognition.},
	urldate = {2014-08-11},
	journal = {Brain research},
	author = {Li, Hongwei and Liang, Aming and Guan, Fangxia and Fan, Ruitai and Chi, Liankai and Yang, Bo},
	month = sep,
	year = {2013},
	pmid = {23916669},
	keywords = {Animals, Cell Survival, Cell Survival: physiology, Exercise Test, Exercise Test: methods, Exercise Test: psychology, Hippocampus, Hippocampus: cytology, Hippocampus: physiology, Male, Maze Learning, Maze Learning: physiology, Memory, Memory: physiology, Mice, Mice, Inbred C57BL, Neurogenesis, Neurogenesis: physiology, Physical Conditioning, Animal, Physical Conditioning, Animal: methods, Physical Conditioning, Animal: physiology, Physical Conditioning, Animal: psychology, Random Allocation, Stress, Psychological, Stress, Psychological: pathology, Stress, Psychological: prevention \& control, Stress, Psychological: psychology},
	pages = {1--8},
}

@article{borst_targeted_2013,
	title = {Targeted radiosensitization by the {Chk1} inhibitor {SAR}-020106},
	volume = {85},
	issn = {1879-355X},
	doi = {10.1016/j.ijrobp.2012.08.006},
	abstract = {PURPOSE: To explore the activity of a potent Chk1 inhibitor (SAR-020106) in combination with radiation.
METHODS AND MATERIALS: Colony and mechanistic in vitro assays and a xenograft in vivo model.
RESULTS: SAR-020106 suppressed-radiation-induced G2/M arrest and reduced clonogenic survival only in p53-deficient tumor cells. SAR-020106 promoted mitotic entry following irradiation in all cell lines, but p53-deficient cells were likely to undergo apoptosis or become aneuploid, while p53 wild-type cells underwent a postmitotic G1 arrest followed by subsequent normal cell cycle re-entry. Following combined treatment with SAR-020106 and radiation, homologous-recombination-mediated DNA damage repair was inhibited in all cell lines. A significant increase in the number of pan-γH2AX-staining apoptotic cells was observed only in p53-deficient cell lines. Efficacy was confirmed in vivo in a clinically relevant human head-and-neck cell carcinoma xenograft model.
CONCLUSION: The Chk1 inhibitor SAR-020106 is a potent radiosensitizer in tumor cell lines defective in p53 signaling.},
	language = {eng},
	number = {4},
	journal = {International Journal of Radiation Oncology, Biology, Physics},
	author = {Borst, Gerben R. and McLaughlin, Martin and Kyula, Joan N. and Neijenhuis, Sari and Khan, Aadil and Good, James and Zaidi, Shane and Powell, Ned G. and Meier, Pascal and Collins, Ian and Garrett, Michelle D. and Verheij, Marcel and Harrington, Kevin J.},
	month = mar,
	year = {2013},
	keywords = {Animals, Apoptosis, Cell Line, Tumor, Cell cycle, Checkpoint Kinase 1, Cyclin-Dependent Kinase Inhibitor p21, DNA Damage, DNA Repair, G2 Phase, HeLa Cells, Histones, Humans, Immunohistochemistry, Isoquinolines, Mice, Mice, Nude, Microscopy, Mitosis, Papillomaviridae, Protein Kinases, Pyrazines, Radiation Tolerance, Radiation-Sensitizing Agents, Time-Lapse Imaging, Tumor Stem Cell Assay, Tumor Suppressor Protein p53},
	pages = {1110--1118},
}

@article{haglund_c-terminal_2013,
	title = {The {C}-terminal peptide of chondroadherin modulates cellular activity by selectively binding to heparan sulfate chains},
	volume = {288},
	issn = {1083-351X},
	doi = {10.1074/jbc.M112.430512},
	abstract = {Chondroadherin, a leucine-rich repeat family member, contains a very C-terminal sequence CKFPTKRSKKAGRH(359), now shown to bind to heparin with a K(D) of 13 μm. This observation led us to investigate whether chondroadherin interacts via this C-terminal heparin-binding domain with glycosaminoglycan chains of proteoglycans at the cell surface. Cells were shown to bind this heparin-binding peptide in FACS analysis, and the interaction was shown to be with glycosaminoglycans because it was abolished when sulfation was inhibited by chlorate treatment of the cells. In separate experiments, heparin and heparan sulfate inhibited the peptide interaction in a dose-dependent manner. Using a human chondrosarcoma and a murine osteoblast cell line, heparan sulfate proteoglycans were identified as the cell surface receptors involved in the binding. Different binding syndecans were identified in the two different cell lines, indicating that the same protein core of a proteoglycan may have structural and functional differences in the attached heparan sulfate chains. Upon binding to coated peptide, cells spread, demonstrating engagement of the cytoskeleton, but no focal adhesion complex was formed. The number of cells adhering via their β(1) integrin receptor to collagen type II or chondroadherin was profoundly and rapidly enhanced by the addition of the heparin-binding peptide. The peptide added to the cells caused ERK phosphorylation, showing that it triggered intracellular signaling. The results show that heparan sulfate chains differ between various members of the proteoglycan families on a given cell, but also differ between the same proteoglycan on different cells with a potential for differential regulation of cellular activities.},
	language = {eng},
	number = {2},
	journal = {The Journal of Biological Chemistry},
	author = {Haglund, Lisbet and Tillgren, Viveka and Önnerfjord, Patrik and Heinegård, Dick},
	month = jan,
	year = {2013},
	pmid = {23172228},
	pmcid = {PMC3543049},
	keywords = {Amino Acid Sequence, Animals, Base Sequence, Calorimetry, Cell Line, Chromatography, Affinity, DNA Primers, Extracellular Matrix, Extracellular Matrix Proteins, Heparitin Sulfate, Humans, Mice, Molecular Sequence Data, Protein Binding, Recombinant Proteins},
	pages = {995--1008},
}

@article{liu_characterization_2013,
	title = {Characterization of {Torin2}, an {ATP}-competitive inhibitor of {mTOR}, {ATM}, and {ATR}},
	volume = {73},
	issn = {1538-7445},
	doi = {10.1158/0008-5472.CAN-12-1702},
	abstract = {mTOR is a highly conserved serine/threonine protein kinase that serves as a central regulator of cell growth, survival, and autophagy. Deregulation of the PI3K/Akt/mTOR signaling pathway occurs commonly in cancer and numerous inhibitors targeting the ATP-binding site of these kinases are currently undergoing clinical evaluation. Here, we report the characterization of Torin2, a second-generation ATP-competitive inhibitor that is potent and selective for mTOR with a superior pharmacokinetic profile to previous inhibitors. Torin2 inhibited mTORC1-dependent T389 phosphorylation on S6K (RPS6KB1) with an EC(50) of 250 pmol/L with approximately 800-fold selectivity for cellular mTOR versus phosphoinositide 3-kinase (PI3K). Torin2 also exhibited potent biochemical and cellular activity against phosphatidylinositol-3 kinase-like kinase (PIKK) family kinases including ATM (EC(50), 28 nmol/L), ATR (EC(50), 35 nmol/L), and DNA-PK (EC(50), 118 nmol/L; PRKDC), the inhibition of which sensitized cells to Irradiation. Similar to the earlier generation compound Torin1 and in contrast to other reported mTOR inhibitors, Torin2 inhibited mTOR kinase and mTORC1 signaling activities in a sustained manner suggestive of a slow dissociation from the kinase. Cancer cell treatment with Torin2 for 24 hours resulted in a prolonged block in negative feedback and consequent T308 phosphorylation on Akt. These effects were associated with strong growth inhibition in vitro. Single-agent treatment with Torin2 in vivo did not yield significant efficacy against KRAS-driven lung tumors, but the combination of Torin2 with mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor AZD6244 yielded a significant growth inhibition. Taken together, our findings establish Torin2 as a strong candidate for clinical evaluation in a broad number of oncologic settings where mTOR signaling has a pathogenic role.},
	language = {eng},
	number = {8},
	journal = {Cancer Research},
	author = {Liu, Qingsong and Xu, Chunxiao and Kirubakaran, Sivapriya and Zhang, Xin and Hur, Wooyoung and Liu, Yan and Kwiatkowski, Nicholas P. and Wang, Jinhua and Westover, Kenneth D. and Gao, Peng and Ercan, Dalia and Niepel, Mario and Thoreen, Carson C. and Kang, Seong A. and Patricelli, Matthew P. and Wang, Yuchuan and Tupper, Tanya and Altabef, Abigail and Kawamura, Hidemasa and Held, Kathryn D. and Chou, Danny M. and Elledge, Stephen J. and Janne, Pasi A. and Wong, Kwok-Kin and Sabatini, David M. and Gray, Nathanael S.},
	month = apr,
	year = {2013},
	keywords = {Adenosine Triphosphate, Animals, Antineoplastic Agents, Apoptosis, Ataxia Telangiectasia Mutated Proteins, Autophagy, Benzimidazoles, Binding, Competitive, Cell Cycle Proteins, Cell Line, Tumor, Cell Proliferation, Cell cycle, DNA-Binding Proteins, Disease Models, Animal, Drug Synergism, Humans, Kinetics, Lung Neoplasms, Mice, Naphthyridines, Protein Binding, Protein Kinase Inhibitors, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Tumor Burden, Tumor Suppressor Proteins, Xenograft Model Antitumor Assays, ras Proteins},
	pages = {2574--2586},
}

@article{cooley_effect_2013,
	title = {The effect of {Msh2} knockdown on toxicity induced by tert-butyl-hydroperoxide, potassium bromate, and hydrogen peroxide in base excision repair proficient and deficient cells},
	volume = {2013},
	issn = {2314-6141},
	doi = {10.1155/2013/152909},
	abstract = {The DNA mismatch repair (MMR) and base excision repair (BER) systems are important determinants of cellular toxicity following exposure to agents that cause oxidative DNA damage. To examine the interactions between these different repair systems, we examined whether toxicity, induced by t-BOOH and KBrO3, differs in BER proficient (Mpg (+/+), Nth1 (+/+)) and deficient (Mpg (-/-), Nth1 (-/-)) mouse embryonic fibroblasts (MEFs) following Msh2 knockdown of between 79 and 88\% using an shRNA expression vector. Msh2 knockdown in Nth1 (+/+) cells had no effect on t-BOOH and KBrO3 induced toxicity as assessed by an MTT assay; knockdown in Nth1 (-/-) cells resulted in increased resistance to t-BOOH and KBrO3, a result consistent with Nth1 removing oxidised pyrimidines. Msh2 knockdown in Mpg (+/+) cells had no effect on t-BOOH toxicity but increased resistance to KBrO3; in Mpg (-/-) cells, Msh2 knockdown increased cellular sensitivity to KBrO3 but increased resistance to t-BOOH, suggesting a role for Mpg in removing DNA damage induced by these agents. MSH2 dependent and independent pathways then determine cellular toxicity induced by oxidising agents. A complex interaction between MMR and BER repair systems, that is, exposure dependent, also exists to determine cellular toxicity.},
	language = {eng},
	journal = {BioMed Research International},
	author = {Cooley, N. and Elder, R. H. and Povey, A. C.},
	year = {2013},
	pmid = {23984319},
	pmcid = {PMC3747367},
	keywords = {Animals, Bromates, Cell Line, Cell Survival, Clone Cells, DNA Glycosylases, DNA Repair, Deoxyribonuclease (Pyrimidine Dimer), Embryo, Mammalian, Fibroblasts, Gene Expression Regulation, Gene Knockdown Techniques, Gene Silencing, Hydrogen Peroxide, Mice, MutS Homolog 2 Protein, tert-Butylhydroperoxide},
	pages = {152909},
}

Paper  doi  abstract   bibtex   

@article{heredia_behavioral_2012,
	title = {Behavioral effects of oral subacute exposure to {BDE}-209 in young adult mice: a preliminary study.},
	volume = {50},
	issn = {1873-6351},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/22178224},
	doi = {10.1016/j.fct.2011.12.002},
	abstract = {In this study, we examined the effects of an oral subacute exposure to 2,2',3,3',4,4',5,5',6,6'-decabromodiphenyl ether (BDE-209) on young adult inbred wild type Tg2576 mice. BDE-209 was administered by gavage at doses of 0 and 20 mg/kg/day dissolved in sunflower oil for 15 days. Two behavioral endpoints were examined: anxiety-activity in a light/dark test and a zero maze test, and learning and spatial memory in a water maze test. Young adult mice exposed to BDE-209 showed a reduction in anxiety levels and a delayed learning in a spatial memory task. Although the results indicated that behavioral effects were present in a young adult exposed population of wild type Tg2576 mice, further studies on chronic exposure to BDE-209 are clearly necessary in order to corroborate these effects.},
	number = {3-4},
	journal = {Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association},
	author = {Heredia, Luis and Torrente, Margarita and Colomina, María T and Domingo, José L},
	month = mar,
	year = {2012},
	pmid = {22178224},
	keywords = {Administration, Animal, Animal: drug effects, Animals, Behavior, Body Weight, Body Weight: drug effects, Darkness, Dose-Response Relationship, Drug, Flame Retardants: pharmacology, Flame retardants, Halogenated Diphenyl Ethers, Halogenated Diphenyl Ethers: pharmacology, Light, Male, Maze Learning, Mice, Oral, Transgenic},
	pages = {707--12},
}

Website  abstract   bibtex   

@article{
 title = {Syndecan-1 promotes the angiogenic phenotype of multiple myeloma endothelial cells.},
 type = {article},
 year = {2012},
 identifiers = {[object Object]},
 keywords = {Animals,Cells, Cultured,Cultured,Endothelium,Endothelium: pathology,Flow Cytometry,Gene Silencing,Humans,Immunoprecipitation,Mice,Multiple Myeloma,Multiple Myeloma: blood supply,Multiple Myeloma: pathology,Neovascularization, Pathologic,Pathologic,Real-Time Polymerase Chain Reaction,Signal Transduction,Syndecan-1,Syndecan-1: genetics,Syndecan-1: physiology,Tumor Cells, Cultured,Vascular Endothelial Growth Factor A,Vascular Endothelial Growth Factor A: metabolism,Vascular Endothelial Growth Factor Receptor-2,Vascular Endothelial Growth Factor Receptor-2: met},
 pages = {1081-90},
 volume = {26},
 websites = {http://dx.doi.org/10.1038/leu.2011.290},
 month = {5},
 publisher = {Macmillan Publishers Limited},
 id = {0dc3a323-ae53-325a-9f8b-74d28f5e217a},
 created = {2016-06-24T20:50:03.000Z},
 accessed = {2014-12-01},
 file_attached = {false},
 profile_id = {954a987f-819f-3985-95a4-2991e0cf0552},
 group_id = {8440dcff-74cc-3783-aef7-fe2749cfc7ef},
 last_modified = {2016-06-24T20:50:03.000Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Lamorte2012},
 short_title = {Leukemia},
 abstract = {Angiogenesis is considered a hallmark of multiple myeloma (MM) progression. In the present study, we evaluated the morphological and functional features of endothelial cells (ECs) derived from bone marrow (BM) of patients affected by MM (MMECs). We found that MMECs compared with normal BM ECs (BMECs) showed increased expression of syndecan-1. Silencing of syndecan-1 expression by RNA interference technique decreased in vitro EC survival, proliferation and organization in capillary-like structures. In vivo, in severe combined immunodeficient mice, syndecan-1 silencing inhibited MMEC organization into patent vessels. When overexpressed in human umbilical vein ECs and BMECs, syndecan-1 induced in vitro and in vivo angiogenic effects. Flow-cytometric analysis of MMECs silenced for syndecan-1 expression indicated a decreased membrane expression of vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2). Immunoprecipitation and confocal analysis showed colocalization of VEGFR-2 with syndecan-1. Absence of nuclear translocation of VEGFR-2 in syndecan-1-knockdown cells together with the shift from perinuclear localization to recycling compartments suggest a role of syndecan-1 in modulation of VEGFR-2 localization. This correlated with an in vitro decreased VEGF-induced invasion and motility. These results suggest that syndecan-1 may contribute to the highly angiogenic phenotype of MMECs by promoting EC proliferation, survival and modulating VEGF-VEGFR-2 signalling.},
 bibtype = {article},
 author = {Lamorte, S and Ferrero, S and Aschero, S and Monitillo, L and Bussolati, B and Omedè, P and Ladetto, M and Camussi, G},
 journal = {Leukemia},
 number = {5}
}

@article{kim_berberine-induced_2012,
	title = {Berberine-induced {AMPK} activation inhibits the metastatic potential of melanoma cells via reduction of {ERK} activity and {COX}-2 protein expression},
	volume = {83},
	issn = {1873-2968},
	doi = {10.1016/j.bcp.2011.11.008},
	abstract = {Berberine is clinically important natural isoquinoline alkaloid that affects various biological functions, such as cell proliferation, migration and survival. The activation of AMP-activated protein kinase (AMPK) regulates tumor cell migration. However, the specific role of AMPK on the metastatic potential of cancer cells remains largely unknown. The present study investigated whether berberine induces AMPK activation and whether this induction directly affects mouse melanoma cell migration, adhesion and invasion. Berberine strongly increased AMPK phosphorylation via reactive oxygen species (ROS) production. 5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), a well-known AMPK activator, also inhibited tumor cell adhesion and invasion and reduced the expression of epithelial to mesenchymal transition (EMT)-related genes. Knockdown of AMPKα subunits using siRNAs significantly abated the berberine-induced inhibition of tumor cell invasion. Furthermore, berberine inhibited the metastatic potential of melanoma cells through a decrease in ERK activity and protein levels of cyclooxygenase-2 (COX-2) by a berberine-induced AMPK activation. These data were confirmed using specific MEK inhibitor, PD98059, and a COX-2 inhibitor, celecoxib. Berberine- and AICAR-treated groups demonstrated significantly decreased lung metastases in the pulmonary metastasis model in vivo. Treatment with berberine also decreased the metastatic potential of A375 human melanoma cells. Collectively, our results suggest that berberine-induced AMPK activation inhibits the metastatic potential of tumor cells through a reduction in the activity of the ERK signaling pathway and COX-2 protein levels.},
	number = {3},
	journal = {Biochemical pharmacology},
	author = {Kim, Hak-Su and Kim, Myung-Jin and Kim, Eun Ju and Yang, Young and Lee, Myeong-Sok and Lim, Jong-Seok},
	month = feb,
	year = {2012},
	pmid = {22120676},
	keywords = {AMP-Activated Protein Kinases, Animals, Berberine, Cell Line, Tumor, Cyclooxygenase 2, Enzyme Activation, Extracellular Signal-Regulated MAP Kinases, Humans, MAP Kinase Signaling System, Melanoma, Experimental, Mice, Mice, Inbred C57BL, Neoplasm Invasiveness},
	pages = {385--394},
}

@article{saunders_nmda_2012,
	title = {{NMDA} antagonists recreate signal-to-noise ratio and timing perturbations present in schizophrenia},
	volume = {46},
	copyright = {All rights reserved},
	issn = {1095-953X},
	doi = {10.1016/j.nbd.2011.12.049},
	abstract = {RATIONALE: There is increasing evidence that functional deficits in schizophrenia may be driven by a reduction in the signal-to-noise ratio (SNR) and consistent timing of neural signals. This study examined the extent to which exposure to the NMDA receptor antagonists ketamine and MK801, frequently used pharmacological models of schizophrenia, recreate deficits in electrophysiological markers of disturbed brain circuits that are thought to underlie the illness. Furthermore, this study characterizes the specificity of these differences across the frequency spectrum so as to help identify the nature of selective circuit abnormalities that mediate each oscillatory response as relevant to schizophrenia.
DESIGN: Mouse EEG was recorded during exposure to repeated auditory stimuli after injection of either vehicle or drug. The dose-response relationship for each electrophysiological measure was determined for ketamine and MK-801. Time-frequency analyses were performed to assess baseline, total, and evoked power and intertrial coherence (ITC) at low (5-10 Hz) and high (35-80 Hz)-frequencies.
RESULTS: High frequency evoked and total power was decreased by MK-801 and ketamine in a dose-dependent fashion. High frequency baseline power was increased by MK-801 and ketamine in a dose-dependent fashion. Similar to evoked power, high frequency inter-trial coherence was dose-dependently decreased by both drugs. Low frequency ITC was only decreased by ketamine.
CONCLUSIONS: Both ketamine and MK-801 cause alterations in high-frequency baseline (noise), total (signal), and evoked (signal) power resulting in a loss of high frequency SNR that is thought to primarily reflect local circuit activity. These changes indicate an inappropriate increase in baseline activity, which can also be interpreted as non-task related activity. Ketamine induced a loss of intertrial coherence at low frequencies, indicating a loss of consistency in low-frequency circuit mechanisms. As a proportion of baseline power, both drugs had a relative shift from low to high frequencies, reflecting a change in the balance of brain activity from coordination of global regions to a pattern of discoordinated, autonomous local activity. These changes are consistent with a pattern of fragmented regional brain activity seen in schizophrenia.},
	language = {eng},
	number = {1},
	journal = {Neurobiology of Disease},
	author = {Saunders, John A. and Gandal, Michael J. and Siegel, Steve J.},
	month = apr,
	year = {2012},
	pmid = {22245663},
	pmcid = {PMC4161042},
	note = {00050 },
	keywords = {Animals, Disease Models, Animal, Evoked Potentials, Excitatory Amino Acid Antagonists, Male, Mice, Mice, Inbred C57BL, Neural Pathways, Receptors, N-Methyl-D-Aspartate, Schizophrenia},
	pages = {93--100}
}

@article{kelly_essential_2011,
	title = {The essential role of evasion from cell death in cancer},
	volume = {111},
	issn = {0065-230X},
	doi = {10.1016/B978-0-12-385524-4.00002-7},
	abstract = {The link between evasion of apoptosis and the development of cellular hyperplasia and ultimately cancer is implicitly clear if one considers how many cells are produced each day and, hence, how many cells must die to make room for the new ones (reviewed in Raff, 1996). Furthermore, cells are frequently experiencing noxious stimuli that can cause lesions in their DNA and faults in DNA replication can occur during cellular proliferation. Such DNA damage needs to be repaired efficiently or cells with irreparable damage must be killed to prevent subsequent division of aberrant cells that may fuel tumorigenesis (reviewed in Weinberg, 2007). The detection of genetic lesions in human cancers that activate prosurvival genes or disable proapoptotic genes have provided the first evidence that defects in programmed cell death can cause cancer (Tagawa et al., 2005; Tsujimoto et al., 1984; Vaux, Cory, and Adams, 1988) and this concept was proven by studies with genetically modified mice (Egle et al., 2004b; Strasser et al., 1990a). It is therefore now widely accepted that evasion of apoptosis is a requirement for both neoplastic transformation and sustained growth of cancer cells (reviewed in Cory and Adams, 2002; Hanahan and Weinberg, 2000; Weinberg, 2007). Importantly, apoptosis is also a major contributor to anticancer therapy-induced killing of tumor cells (reviewed in Cory and Adams, 2002; Cragg et al., 2009). Consequently, a detailed understanding of apoptotic cell death will help to better comprehend the complexities of tumorigenesis and should assist with the development of improved targeted therapies for cancer based on the direct activation of the apoptotic machinery (reviewed in Lessene, Czabotar, and Colman, 2008).},
	language = {eng},
	journal = {Advances in Cancer Research},
	author = {Kelly, Gemma L. and Strasser, Andreas},
	year = {2011},
	keywords = {Animals, Cell Death, Humans, Mice, Neoplasms},
	pages = {39--96},
}

@article{leichtle_innate_2011,
	title = {Innate signaling in otitis media: pathogenesis and recovery},
	volume = {11},
	issn = {1534-6315},
	shorttitle = {Innate signaling in otitis media},
	doi = {10.1007/s11882-010-0158-3},
	abstract = {Otitis media (OM) is the most prevalent childhood disease in developed countries. Involvement of innate immunity mediated by Toll-like receptors (TLRs) in OM has been implicated primarily in cell lines and by association studies of innate immune gene polymorphisms with OM prevalence. However, the precise role of innate immunity in OM is incompletely understood. We review recent research that has advanced our understanding of how innate immunity in the middle ear is mediated by the interaction of pathogen molecules with receptors such as the TLRs, leading to the activation of adaptor molecules and production of proinflammatory cytokines. TLR genes and signaling molecules are upregulated in OM in a murine model. Deletion of several key innate immune genes results in persistent OM in mice, coupled with an inability to clear bacterial infection from the middle ear. It is concluded that an intact innate immune signaling system is critical to recovery from bacterial OM.},
	language = {eng},
	number = {1},
	journal = {Current Allergy and Asthma Reports},
	author = {Leichtle, Anke and Lai, Yuping and Wollenberg, Barbara and Wasserman, Stephen I. and Ryan, Allen F.},
	month = feb,
	year = {2011},
	pmid = {21049294},
	pmcid = {PMC3020300},
	keywords = {Animals, Child, Cytokines, Haemophilus Infections, Haemophilus influenzae, Humans, Immunity, Innate, Mice, Otitis Media, Signal Transduction, Toll-Like Receptor 2, Toll-Like Receptor 4, Toll-Like Receptors, Tumor Necrosis Factor-alpha},
	pages = {78--84},
}

@article{hancock_copper_2011,
	title = {A copper chelate of thiosemicarbazone {NSC} 689534 induces oxidative/{ER} stress and inhibits tumor growth in vitro and in vivo},
	volume = {50},
	issn = {1873-4596},
	doi = {10.1016/j.freeradbiomed.2010.10.696},
	abstract = {In this study, a Cu(2+) chelate of the novel thiosemicarbazone NSC 689534 was evaluated for in vitro and in vivo anti-cancer activity. Results demonstrated that NSC 689534 activity (low micromolar range) was enhanced four- to fivefold by copper chelation and completely attenuated by iron. Importantly, once formed, the NSC 689534/Cu(2+) complex retained activity in the presence of additional iron or iron-containing biomolecules. NSC 689534/Cu(2+) mediated its effects primarily through the induction of ROS, with depletion of cellular glutathione and protein thiols. Pretreatment of cells with the antioxidant N-acetyl-l-cysteine impaired activity, whereas NSC 689534/Cu(2+) effectively synergized with the glutathione biosynthesis inhibitor buthionine sulfoximine. Microarray analysis of NSC 689534/Cu(2+)-treated cells highlighted activation of pathways involved in oxidative and ER stress/UPR, autophagy, and metal metabolism. Further scrutiny of the role of ER stress and autophagy indicated that NSC 689534/Cu(2+)-induced cell death was ER-stress dependent and autophagy independent. Last, NSC 689534/Cu(2+) was shown to have activity in an HL60 xenograft model. These data suggest that NSC 689534/Cu(2+) is a potent oxidative stress inducer worthy of further preclinical investigation.},
	language = {eng},
	number = {1},
	journal = {Free Radical Biology \& Medicine},
	author = {Hancock, Chad N. and Stockwin, Luke H. and Han, Bingnan and Divelbiss, Raymond D. and Jun, Jung Ho and Malhotra, Sanjay V. and Hollingshead, Melinda G. and Newton, Dianne L.},
	month = jan,
	year = {2011},
	pmid = {20971185},
	pmcid = {PMC3014388},
	keywords = {Animals, Antineoplastic Agents, Cell Proliferation, Chelating Agents, Copper, Down-Regulation, Endoplasmic Reticulum, Female, HL-60 Cells, Humans, Mice, Mice, Nude, Neoplasms, Organometallic Compounds, Oxidants, Oxidative Stress, Thiosemicarbazones, Tumor Cells, Cultured, Unfolded Protein Response, Up-Regulation, Xenograft Model Antitumor Assays},
	pages = {110--121},
}

Paper  doi  abstract   bibtex   

@article{viberg_differences_2011,
	title = {Differences in neonatal neurotoxicity of brominated flame retardants, {PBDE} 99 and {TBBPA}, in mice.},
	volume = {289},
	issn = {1879-3185},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/21820030},
	doi = {10.1016/j.tox.2011.07.010},
	abstract = {Flame retardants such as polybrominated diphenyl ethers (PBDE) and tetrabromobisphenol A are used as flame retardants and detected in the environmental, wildlife species and human tissues. Exposure to PBDEs during the neonatal development of the brain has been shown to affect behavior and learning and memory in adult mice, while neonatal exposure to TBBPA (another brominated flame retardant) did not affect behavioral variables in the adult. In this study, we hypothesized that the effects of these compounds could be reflected by changes in biochemical substrates and cholinergic receptors and have examined the levels of four proteins involved in maturation of the brain, neuronal growth and synaptogenesis and the densities of both muscarinic and nicotinic cholinergic receptors. We measured the levels of radioactivity in the brain after administration of (14)C-labelled TBBPA at different time points and saw that levels of TBBA peaked earlier and decreased faster than the earlier reported levels of PBDE 99. The protein analysis in the neonatal brain showed changes in the levels of calcium/calmodulin-dependent protein kinase II (CaMKII), growth associated protein-43 (GAP-43) and synaptophysin following neonatal exposure to PBDE 99 (21 μmol/kg body weight), but not following exposure TBBPA. Furthermore, neonatal exposure to PBDE 99 and TBBPA caused a decrease in binding sites of the nicotinic ligand cytisine in frontal cortex. These results confirm earlier reported data that PBDE 99 can act as a developmental neurotoxicant, possibly due to its different uptake and retention in the brain compared to TBBPA. In addition, the changes in protein levels are interesting leads in the search for mechanisms behind the developmental neonatal neurotoxicity of PBDEs in general and PBDE 99 in particular, since also other compounds inducing similar adult behavioral disturbances as PBDE 99, affect these proteins during the period of rapid brain development.},
	number = {1},
	journal = {Toxicology},
	author = {Viberg, Henrik and Eriksson, Per},
	month = oct,
	year = {2011},
	pmid = {21820030},
	keywords = {Alkaloids, Alkaloids: metabolism, Animals, Azocines, Azocines: metabolism, Brain, Brain: drug effects, Brain: metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Flame Retardants: toxicity, Flame retardants, GAP-43 Protein, GAP-43 Protein: metabolism, Halogenated Diphenyl Ethers, Halogenated Diphenyl Ethers: toxicity, Immunoblotting, Male, Mice, Neurotoxicity Syndromes, Neurotoxicity Syndromes: etiology, Neurotoxicity Syndromes: metabolism, Newborn, Polybrominated Biphenyls, Polybrominated Biphenyls: toxicity, Quinolizines, Quinolizines: metabolism, Synaptophysin, Synaptophysin: metabolism, unsure},
	pages = {59--65},
}

@article{navarro_phosphoproteomic_2011,
	title = {Phosphoproteomic analysis reveals an intrinsic pathway for the regulation of histone deacetylase 7 that controls the function of cytotoxic {T} lymphocytes},
	volume = {12},
	issn = {1529-2916},
	doi = {10.1038/ni.2008},
	abstract = {Here we report an unbiased analysis of the cytotoxic T lymphocyte (CTL) serine-threonine phosphoproteome by high-resolution mass spectrometry. We identified approximately 2,000 phosphorylations in CTLs, of which approximately 450 were controlled by T cell antigen receptor (TCR) signaling. A significantly overrepresented group of molecules identified included transcription activators, corepressors and chromatin regulators. A focus on chromatin regulators showed that CTLs had high expression of the histone deacetylase HDAC7 but continually phosphorylated and exported this transcriptional repressor from the nucleus. Dephosphorylation of HDAC7 resulted in its accumulation in the nucleus and suppressed expression of genes encoding key cytokines, cytokine receptors and adhesion molecules that determine CTL function. Screening of the CTL phosphoproteome has thus identified intrinsic pathways of serine-threonine phosphorylation that target chromatin regulators and determine the CTL functional program.},
	language = {eng},
	number = {4},
	journal = {Nature Immunology},
	author = {Navarro, Maria N. and Goebel, Jurgen and Feijoo-Carnero, Carmen and Morrice, Nick and Cantrell, Doreen A.},
	month = apr,
	year = {2011},
	pmid = {21399638},
	pmcid = {PMC3110993},
	keywords = {Amino Acid Sequence, Animals, Antigen, Cell Nucleus, Cells, Chromatography, Confocal, Cultured, Cytosol, Cytotoxic, DAG, Female, Gene Expression Profiling, Green Fluorescent Proteins, Histone Deacetylases, Inbred C57BL, Liquid, Male, Mass Spectrometry, Mice, Microscopy, Molecular Sequence Data, Oligonucleotide Array Sequence Analysis, Phosphoproteins, Phosphorylation, Proteomics, Receptors, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, T-Cell, T-Lymphocytes, Transgenic},
	pages = {352--361}
}

@article{hussein_pediatric_2011,
	title = {Pediatric brain tumor cancer stem cells: cell cycle dynamics, {DNA} repair, and etoposide extrusion},
	volume = {13},
	issn = {1523-5866},
	shorttitle = {Pediatric brain tumor cancer stem cells},
	doi = {10.1093/neuonc/noq144},
	abstract = {Reliable model systems are needed to elucidate the role cancer stem cells (CSCs) play in pediatric brain tumor drug resistance. The majority of studies to date have focused on clinically distinct adult tumors and restricted tumor types. Here, the CSC component of 7 newly established primary pediatric cell lines (2 ependymomas, 2 medulloblastomas, 2 gliomas, and a CNS primitive neuroectodermal tumor) was thoroughly characterized. Comparison of DNA copy number with the original corresponding tumor demonstrated that genomic changes present in the original tumor, typical of that particular tumor type, were retained in culture. In each case, the CSC component was approximately 3-4-fold enriched in neurosphere culture compared with monolayer culture, and a higher capacity for multilineage differentiation was observed for neurosphere-derived cells. DNA content profiles of neurosphere-derived cells expressing the CSC marker nestin demonstrated the presence of cells in all phases of the cell cycle, indicating that not all CSCs are quiescent. Furthermore, neurosphere-derived cells demonstrated an increased resistance to etoposide compared with monolayer-derived cells, having lower initial DNA damage, potentially due to a combination of increased drug extrusion by ATP-binding cassette multidrug transporters and enhanced rates of DNA repair. Finally, orthotopic xenograft models reflecting the tumor of origin were established from these cell lines. In summary, these cell lines and the approach taken provide a robust model system that can be used to develop our understanding of the biology of CSCs in pediatric brain tumors and other cancer types and to preclinically test therapeutic agents.},
	language = {eng},
	number = {1},
	journal = {Neuro-Oncology},
	author = {Hussein, Deema and Punjaruk, Wiyada and Storer, Lisa C. D. and Shaw, Lucy and Othman, Ramadhan and Ottoman, Ramadan and Peet, Andrew and Miller, Suzanne and Bandopadhyay, Gagori and Heath, Rachel and Kumari, Rajendra and Bowman, Karen J. and Braker, Paul and Rahman, Ruman and Jones, George D. D. and Watson, Susan and Lowe, James and Kerr, Ian D. and Grundy, Richard G. and Coyle, Beth},
	month = jan,
	year = {2011},
	keywords = {Adolescent, Animals, Antineoplastic Agents, Phytogenic, Brain Neoplasms, Cell cycle, Child, Child, Preschool, Chromosome Aberrations, DNA Repair, Drug Resistance, Neoplasm, Etoposide, Glioblastoma, Humans, Mice, Neoplasm Recurrence, Local, Neoplastic Stem Cells, Polymorphism, Single Nucleotide, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, comet assay},
	pages = {70--83},
}

@article{ mutlu_effects_2011,
  title = {Effects of nitric oxide synthase inhibitors 1-(2-trifluoromethylphenyl)--imidazole ({TRIM}) and 7-nitroindazole (7-{NI}) on learning and memory in mice},
  volume = {25},
  issn = {1472-8206},
  doi = {10.1111/j.1472-8206.2010.00851.x},
  abstract = {Nitric oxide ({NO}) plays an important role in hippocampal long-term potentiation ({LTP}), which is involved in memory processes. This led to the hypothesis that nitric oxide synthase ({NOS}) inhibitors will have disturbing effects on learning and memory. The aim of our study was to investigate the effects of the new selective neuronal and inducible {NOS} inhibitor 1- (2-trifluoromethylphenyl) imidazole ({TRIM}) (10-50 mg/kg) on learning and memory and compare it to the nonselective {NOS} inhibitor 7-{NI} (15-45 mg/kg) using different behavioral tests in Swiss mice, thus clarifying the role of neuronal {NOS} ({nNOS}) and endothelial {NOS} ({eNOS}) in cognitive processes. {TRIM} had no specific effect on either learning or memory parameters, while 7-{NI} (30 mg/kg) disturbed spatial memory in the probe trial of the Morris water maze test, which was performed on the last day of the test. No differences between {TRIM} and the control groups were observed, while 7-{NI} (30 and 45 mg/kg) significantly disturbed memory in the novel object recognition test. In the social transmission of food preference test, both {TRIM} (50 mg/kg) and 7-{NI} (45 mg/kg) impaired hippocampal olfactory memory, but the total food consumption was also significantly decreased at these doses. In the passive avoidance test, {TRIM} did not disturb the performance, while memory impairment was observed, even with lower doses of 7-{NI}. All of these results suggest that {TRIM} has no clear effect on cognitive impairment compared to 7-{NI} and that inhibition of both {nNOS} and {eNOS} are necessary for the deterioration of memory processes.},
  language = {eng},
  number = {3},
  journal = {Fundamental \& Clinical Pharmacology},
  author = {Mutlu, Oguz and Ulak, Güner and Belzung, Catherine},
  month = {June},
  year = {2011},
  pmid = {20608991},
  keywords = {Animals, Enzyme Inhibitors, Food Preferences, Hippocampus, Imidazoles, Indazoles, Learning, Locomotion, Long-Term Potentiation, Male, Maze Learning, Memory, Mice, Nitric Oxide Synthase Type I, Nitric Oxide Synthase Type {III}},
  pages = {368--377}
}

@article{li_essential_2011,
	title = {Essential roles of enteric neuronal serotonin in gastrointestinal motility and the development/survival of enteric dopaminergic neurons},
	volume = {31},
	issn = {1529-2401},
	doi = {10.1523/JNEUROSCI.6684-10.2011},
	abstract = {The gut contains a large 5-HT pool in enterochromaffin (EC) cells and a smaller 5-HT pool in the enteric nervous system (ENS). During development, enteric neurons are generated asynchronously. We tested hypotheses that serotonergic neurons, which arise early, affect development/survival of later-born dopaminergic, GABAergic, nitrergic, and calcitonin gene-related peptide-expressing neurons and are essential for gastrointestinal motility. 5-HT biosynthesis depends on tryptophan hydroxylase 1 (TPH1) in EC cells and on TPH2 in neurons; therefore, mice lacking TPH1 and/or TPH2 distinguish EC-derived from neuronal 5-HT. Deletion of TPH2, but not TPH1, decreased myenteric neuronal density and proportions of dopaminergic and GABAergic neurons but did not affect the extrinsic sympathetic innervation of the gut; intestinal transit slowed in mice lacking TPH2 mice, but gastric emptying accelerated. Isolated enteric crest-derived cells (ENCDCs) expressed the serotonin reuptake transporter (SERT) and 15 subtypes of 5-HT receptor. Addition of 5-HT to cultures of isolated ENCDCs promoted total and dopaminergic neuronal development. Rings of SERT-immunoreactive terminal axons surrounded myenteric dopaminergic neurons and SERT knock-out increased intestinal levels of dopamine metabolites, implying that enteric dopaminergic neurons receive a serotonergic innervation. Observations suggest that constitutive gastrointestinal motility depends more on neuronal than EC cell serotonin; moreover, serotonergic neurons promote development/survival of some classes of late-born enteric neurons, including dopaminergic neurons, which appear to innervate and activate in the adult ENS.},
	language = {eng},
	number = {24},
	journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience},
	author = {Li, Zhishan and Chalazonitis, Alcmène and Huang, Yung-Yu and Mann, J. John and Margolis, Kara Gross and Yang, Qi Melissa and Kim, Dolly O. and Côté, Francine and Mallet, Jacques and Gershon, Michael D.},
	month = jun,
	year = {2011},
	pmid = {21677183},
	pmcid = {PMC4442094},
	keywords = {Animals, Calcitonin Gene-Related Peptide, Dopamine, ELAV Proteins, ELAV-Like Protein 3, Embryo, Mammalian, Enteric Nervous System, Enzyme Inhibitors, Gastric Emptying, Gastrointestinal Motility, Gene Expression Regulation, Developmental, Homovanillic Acid, In Vitro Techniques, Intestine, Small, Mice, Mice, Inbred C57BL, Myenteric Plexus, Neurons, Nitric Oxide Synthase Type I, Serotonin, Serotonin Plasma Membrane Transport Proteins, Tryptophan Hydroxylase, Tyrosine 3-Monooxygenase, gamma-Aminobutyric Acid},
	pages = {8998--9009},
}

@article{spyrou_compounds_2010,
	title = {Compounds of the anthracycline family of antibiotics elevate human gamma-globin expression both in erythroid cultures and in a transgenic mouse model.},
	volume = {44},
	copyright = {Copyright (c) 2009 Elsevier Inc. All rights reserved.},
	issn = {1096-0961 1079-9796},
	doi = {10.1016/j.bcmd.2009.10.008},
	language = {eng},
	number = {2},
	journal = {Blood cells, molecules \& diseases},
	author = {Spyrou, Pandelis and Phylactides, Marios and Lederer, Carsten W. and Kithreotis, Lucas and Kirri, Andriani and Christou, Soteroulla and Kkolou, Elena and Kanavakis, Emanuel and Anagnou, Nicholas P. and Stamatoyannopoulos, George and Kleanthous, Marina},
	month = apr,
	year = {2010},
	pmid = {19914848},
	note = {Place: United States},
	keywords = {Animals, Anthracyclines/administration \& dosage/*pharmacology, Anti-Bacterial Agents/administration \& dosage/*pharmacology, Cell Line, Cells, Cultured, Erythroid Cells/drug effects, Fetal Hemoglobin/genetics/metabolism, Gene Expression Regulation/*drug effects, Humans, Mice, Mice, Transgenic, Promoter Regions, Genetic/drug effects, RNA, Messenger/genetics, Thalassemia/drug therapy/genetics, beta-Globins/genetics, gamma-Globins/*genetics},
	pages = {100--106},
}

Paper  doi  abstract   bibtex   

@article{,
   abstract = {In the United States, cancer is the second most common cause of death and it is expected that about 562,340 Americans will have died of cancer in 2009. Bone cancer pain is common in patients with advanced breast, prostate, and lung cancer as these tumors have a remarkable affinity to metastasize to bone. Once tumors metastasize to bone, they are a major cause of morbidity and mortality as the tumor induces significant skeletal remodeling, fractures, pain, and anemia. Currently, the factors that drive cancer pain are poorly understood. However, several recently introduced models of bone cancer pain, which closely mirror the human condition, are providing insight into the mechanisms that drive bone cancer pain and guide the development of mechanism-based therapies to treat the cancer pain. Several of these mechanism-based therapies have now entered human clinical trials. If successful, these therapies have the potential to significantly enlarge the repertoire of modalities that can be used to treat bone cancer pain and improve the quality of life, functional status, and survival of patients with bone cancer. © 2010 New York Academy of Sciences.},
   author = {Juan Miguel Jimenez-Andrade and William G. Mantyh and Aaron P. Bloom and Alice S. Ferng and Christopher P. Geffre and Patrick W. Mantyh},
   doi = {10.1111/J.1749-6632.2009.05429.X},
   isbn = {9781573317788},
   issn = {1749-6632},
   journal = {Annals of the New York Academy of Sciences},
   keywords = {Acidosis / etiology,Animal,Animals,Bone Neoplasms / epidemiology,Bone Neoplasms / mortality,Bone Neoplasms / pathology,Bone Neoplasms / physiopathology*,Bone Neoplasms / secondary,Bone and Bones / pathology,Breast Neoplasms / complications,Disease Models,Female,Humans,Juan Miguel Jimenez-Andrade,Lung Neoplasms / complications,MEDLINE,Male,Mice,NCBI,NIH,NLM,National Center for Biotechnology Information,National Institutes of Health,National Library of Medicine,Neoplasm Metastasis / pathology,Osteoclasts / pathology,PMC5642911,Pain / etiology,Pain / physiopathology*,Patrick W Mantyh,Prostatic Neoplasms / complications,PubMed Abstract,Review,Sarcoma / pathology,United States / epidemiology,William G Mantyh,doi:10.1111/j.1749-6632.2009.05429.x,pmid:20536932},
   pages = {173-181},
   pmid = {20536932},
   publisher = {Ann N Y Acad Sci},
   title = {Bone cancer pain},
   volume = {1198},
   url = {https://pubmed.ncbi.nlm.nih.gov/20536932/},
   year = {2010},
}

@article{guihard_mapk_2010,
	title = {The {MAPK} {ERK1} is a negative regulator of the adult steady-state splenic erythropoiesis},
	volume = {115},
	issn = {1528-0020},
	doi = {10.1182/blood-2009-09-242487},
	abstract = {The mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 1 (ERK1) and ERK2 are among the main signal transduction molecules, but little is known about their isoform-specific functions in vivo. We have examined the role of ERK1 in adult hematopoiesis with ERK1(-/-) mice. Loss of ERK1 resulted in an enhanced splenic erythropoiesis, characterized by an accumulation of erythroid progenitors in the spleen, without any effect on the other lineages or on bone marrow erythropoiesis. This result suggests that the ablation of ERK1 induces a splenic stress erythropoiesis phenotype. However, the mice display no anemia. Deletion of ERK1 did not affect erythropoietin (EPO) serum levels or EPO/EPO receptor signaling and was not compensated by ERK2. Splenic stress erythropoiesis response has been shown to require bone morphogenetic protein 4 (BMP4)-dependent signaling in vivo and to rely on the expansion of a resident specialized population of erythroid progenitors, termed stress erythroid burst-forming units (BFU-Es). A great expansion of stress BFU-Es and increased levels of BMP4 mRNA were found in ERK1(-/-) spleens. The ERK1(-/-) phenotype can be transferred by bone marrow cells. These findings show that ERK1 controls a BMP4-dependent step, regulating the steady state of splenic erythropoiesis.},
	language = {eng},
	number = {18},
	journal = {Blood},
	author = {Guihard, Soizic and Clay, Denis and Cocault, Laurence and Saulnier, Nathalie and Opolon, Paule and Souyri, Michèle and Pagès, Gilles and Pouysségur, Jacques and Porteu, Françoise and Gaudry, Murielle},
	month = may,
	year = {2010},
	keywords = {Anemia, Animals, Apoptosis, Blotting, Western, Bone Marrow Transplantation, Bone Morphogenetic Protein 4, Colony-Forming Units Assay, Erythroid Precursor Cells, Erythropoiesis, Erythropoietin, Flow Cytometry, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase 3, Oxidants, Phenylhydrazines, RNA, Messenger, Receptors, Erythropoietin, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, spleen},
	pages = {3686--3694},
}

Paper  doi  abstract   bibtex   

@article{Sun2010,
	title = {Stable anticancer gold({III})-porphyrin complexes: effects of porphyrin structure.},
	volume = {16},
	issn = {1521-3765},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/20162647},
	doi = {10.1002/chem.200902741},
	abstract = {In the design of physiologically stable anticancer gold(III) complexes, we have employed strongly chelating porphyrinato ligands to stabilize a gold(III) ion [Chem. Commun. 2003, 1718; Coord. Chem. Rev. 2009, 253, 1682]. In this work, a family of gold(III) tetraarylporphyrins with porphyrinato ligands containing different peripheral substituents on the meso-aryl rings were prepared, and these complexes were used to study the structure-bioactivity relationship. The cytotoxic IC(50) values of [Au(Por)](+) (Por=porphyrinato ligand), which range from 0.033 to ¿100 microM, correlate with their lipophilicity and cellular uptake. Some of them induce apoptosis and display preferential cytotoxicity toward cancer cells than to normal noncancerous cells. A new gold(III)-porphyrin with saccharide conjugation [Au(4-glucosyl-TPP)]Cl (2a; H(2)(4-glucosyl-TPP)=meso-tetrakis(4-beta-D-glucosylphenyl)porphyrin) exhibits significant cytostatic activity to cancer cells (IC(50)=1.2-9.0 microM) without causing cell death and is much less toxic to lung fibroblast cells (IC(50)¿100 microM). The gold(III)-porphyrin complexes induce S-phase cell-cycle arrest of cancer cells as indicated by flow cytometric analysis, suggesting that the anticancer activity may be, in part, due to termination of DNA replication. The gold(III)-porphyrin complexes can bind to DNA in vitro with binding constants in the range of 4.9 x 10(5) to 4.1 x 10(6) dm(3) mol(-1) as determined by absorption titration. Complexes 2a and [Au(TMPyP)]Cl(5) (4a; [H(2)TMPyP](4+)=meso-tetrakis(N-methylpyridinium-4-yl)porphyrin) interact with DNA in a manner similar to the DNA intercalator ethidium bromide as revealed by gel mobility shift assays and viscosity measurements. Both of them also inhibited the topoisomerase I induced relaxation of supercoiled DNA. Complex 4a, a gold(III) derivative of the known G-quadruplex-interactive porphyrin [H(2)TMPyP](4+), can similarly inhibit the amplification of a DNA substrate containing G-quadruplex structures in a polymerase chain reaction stop assay. In contrast to these reported complexes, complex 2a and the parental gold(III)-porphyrin 1a do not display a significant inhibitory effect (¡10\%) on telomerase. Based on the results of protein expression analysis and computational docking experiments, the anti-apoptotic bcl-2 protein is a potential target for those gold(III)-porphyrin complexes with apoptosis-inducing properties. Complex 2a also displays prominent anti-angiogenic properties in vitro. Taken together, the enhanced stabilization of the gold(III) ion and the ease of structural modification render porphyrins an attractive ligand system in the development of physiologically stable gold(III) complexes with anticancer and anti-angiogenic activities.},
	number = {10},
	journal = {Chemistry (Weinheim an der Bergstrasse, Germany)},
	author = {Sun, Raymond Wai-Yin and Li, Carrie Ka-Lei and Ma, Dik-Lung and Yan, Jessie Jing and Lok, Chun-Nam and Leung, Chung-Hang and Zhu, Nianyong and Che, Chi-Ming},
	month = mar,
	year = {2010},
	pmid = {20162647},
	keywords = {\#nosource, Animals, Antineoplastic Agents, Antineoplastic Agents: chemistry, Antineoplastic Agents: pharmacology, Binding Sites, Cell Cycle, Cell Cycle: drug effects, Cell Line, Crystallography, DNA, DNA: chemistry, DNA: metabolism, G-Quadruplexes, G-Quadruplexes: drug effects, Gold, Gold: chemistry, Gold: pharmacology, Humans, Ligands, Mice, Organogold Compounds, Organogold Compounds: chemistry, Organogold Compounds: pharmacology, Porphyrins, Porphyrins: chemistry, Porphyrins: metabolism, Porphyrins: pharmacology, Tumor, X-Ray},
	pages = {3097--113},
}

Paper  doi  abstract   bibtex   

@article{Piatkevich2010,
	title = {Monomeric red fluorescent proteins with a large {Stokes} shift.},
	volume = {107},
	issn = {1091-6490},
	url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2851791&tool=pmcentrez&rendertype=abstract},
	doi = {10.1073/pnas.0914365107},
	abstract = {Two-photon microscopy has advanced fluorescence imaging of cellular processes in living animals. Fluorescent proteins in the blue-green wavelength range are widely used in two-photon microscopy; however, the use of red fluorescent proteins is limited by the low power output of Ti-Sapphire lasers above 1,000 nm. To overcome this limitation we have developed two red fluorescent proteins, LSS-mKate1 and LSS-mKate2, which possess large Stokes shifts with excitation/emission maxima at 463/624 and 460/605 nm, respectively. These LSS-mKates are characterized by high pH stability, photostability, rapid chromophore maturation, and monomeric behavior. They lack absorbance in the green region, providing an additional red color to the commonly used red fluorescent proteins. Substantial overlap between the two-photon excitation spectra of the LSS-mKates and blue-green fluorophores enables multicolor imaging using a single laser. We applied this approach to a mouse xenograft model of breast cancer to intravitally study the motility and Golgi-nucleus alignment of tumor cells as a function of their distance from blood vessels. Our data indicate that within 40 mum the breast cancer cells show significant polarization towards vessels in living mice.},
	number = {12},
	urldate = {2013-08-09},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	author = {Piatkevich, Kiryl D and Hulit, James and Subach, Oksana M and Wu, Bin and Abdulla, Arian and Segall, Jeffrey E and Verkhusha, Vladislav V},
	month = mar,
	year = {2010},
	pmid = {20212155},
	keywords = {\#nosource, Amino Acid Substitution, Animals, Cell Line, Tumor, Cell Nucleus, Cell Nucleus: metabolism, Female, Golgi Apparatus, Golgi Apparatus: metabolism, HeLa Cells, Humans, Luminescent Proteins, Luminescent Proteins: chemistry, Luminescent Proteins: genetics, Luminescent Proteins: metabolism, Mammary Neoplasms, Experimental, Mammary Neoplasms, Experimental: blood supply, Mammary Neoplasms, Experimental: genetics, Mammary Neoplasms, Experimental: metabolism, Mice, Microscopy, Fluorescence, Multiphoton, Mutagenesis, Neoplasm Transplantation, Photochemical Processes, Rats, Recombinant Fusion Proteins, Recombinant Fusion Proteins: chemistry, Recombinant Fusion Proteins: genetics, Recombinant Fusion Proteins: metabolism, Transplantation, Heterologous},
	pages = {5369--74},
}

Paper  doi  abstract   bibtex   

@article{Delalande2010,
abstract = {Our study aimed at evaluating the use of ultrasound-assisted microbubbles gene transfer in mice Achilles tendons. Using a plasmid encoding luciferase gene, it was found that an efficient and stable gene expression for more than two weeks was obtained when tendons were injected with 10 microg of plasmid in the presence of 5x10(5) BR14 microbubbles with the following acoustic parameters: 1 MHz, 200 kPa, 40\% duty cycle and 10 min of exposure time. The rate of gene expression was 100-fold higher than that obtained with naked plasmid injected alone without ultrasound or with ultrasound in absence of microbubbles. The long term expression of transgene makes ultrasound-assisted microbubble a suitable method for gene therapy in tendons.},
author = {Delalande, Anthony and Bureau, Michel-Francis and Midoux, Patrick and Bouakaz, Ayache and Pichon, Chantal},
doi = {10.1016/j.ultras.2009.09.035},
file = {:C$\backslash$:/Users/emnicolas/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Delalande et al. - 2010 - Ultrasound-assisted microbubbles gene transfer in tendons for gene therapy.pdf:pdf},
issn = {1874-9968},
journal = {Ultrasonics},
keywords = {Achilles Tendon,Animals,Contrast Media,Contrast Media: chemistry,Equipment Design,Fluorocarbons,Fluorocarbons: chemistry,Gene Expression,Gene Transfer Techniques,Genetic Therapy,Genetic Therapy: methods,Luciferases, Firefly,Luciferases, Firefly: genetics,Mice,Microbubbles,Phospholipids,Phospholipids: chemistry,Plasmids,Plasmids: administration \& dosage,Statistics, Nonparametric,Transfection,Ultrasonics},
month = feb,
number = {2},
pages = {269--72},
pmid = {19857885},
publisher = {Elsevier B.V.},
title = {{Ultrasound-assisted microbubbles gene transfer in tendons for gene therapy.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19857885},
volume = {50},
year = {2010}
}

Paper  abstract   bibtex   

@article{Esposito2009,
  abstract = {Fluorescence microscopy is a non-invasive technique that allows high
	resolution imaging of cytoskeletal structures. Advances in the field
	of fluorescent labelling (e.g., fluorescent proteins, quantum dots,
	tetracystein domains) and optics (e.g., super-resolution techniques
	and quantitative methods) not only provide better images of the cytoskeleton,
	but also offer an opportunity to quantify the complex of molecular
	events that populate this highly organised, yet dynamic, structure.For
	instance, fluorescence lifetime imaging microscopy and Forster resonance
	energy transfer imaging allow mapping of protein-protein interactions;
	furthermore, techniques based on the measurement of photobleaching
	kinetics (e.g., fluorescence recovery after photobleaching, fluorescence
	loss in photobleaching, and fluorescence localisation after photobleaching)
	permit the characterisation of axonal transport and, more generally,
	diffusion of relevant biomolecules.Quantitative fluorescence microscopy
	techniques offer powerful tools for understanding the physiological
	and pathological roles of molecular machineries in the living cell.},
  added-at = {2010-12-14T18:12:02.000+0100},
  author = {Esposito, A. and Schlachter, S. and Schierle, G. S. and Elder, A. D. and Diaspro, A. and Wouters, F. S. and Kaminski, C. F. and Iliev, A. I.},
  biburl = {http://www.bibsonomy.org/bibtex/2e233c6531b3b38c0e14016d30b887410/pharmawuerz},
  endnotereftype = {Journal Article},
  interhash = {f0c57923ba9d698668d19dcc5a81ab70},
  intrahash = {e233c6531b3b38c0e14016d30b887410},
  issn = {1940-6029 (Electronic) 1940-6029 (Linking)},
  journal = {Methods Mol Biol},
  keywords = {imported},
  note = {Esposito, Alessandro Schlachter, Simon Schierle, Gabriele S Kaminski
	Elder, Alan D Diaspro, Alberto Wouters, Fred S Kaminski, Clemens
	F Iliev, Asparouh I Biotechnology and Biological Sciences Research
	Council/United Kingdom Research Support, Non-U.S. Gov't United States
	Methods in molecular biology (Clifton, N.J.) Methods Mol Biol. 2009;586:117-42.},
  pages = {117-42},
  shorttitle = {Quantitative fluorescence microscopy techniques},
  timestamp = {2010-12-14T18:12:10.000+0100},
  title = {Quantitative fluorescence microscopy techniques},
  url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19768427},
  volume = 586,
  year = 2009
}

Paper  Website  abstract   bibtex   

@article{
 title = {Retinoic acid promotes limb induction through effects on body axis extension but is unnecessary for limb patterning.},
 type = {article},
 year = {2009},
 identifiers = {[object Object]},
 keywords = {Aldehyde Oxidoreductases,Aldehyde Oxidoreductases: genetics,Aldehyde Oxidoreductases: metabolism,Animals,Body Patterning,Body Patterning: physiology,Embryo, Mammalian,Embryo, Mammalian: anatomy & histology,Embryo, Mammalian: drug effects,Embryo, Mammalian: physiology,Embryonic Induction,Extremities,Extremities: anatomy & histology,Extremities: embryology,Fibroblast Growth Factor 8,Fibroblast Growth Factor 8: genetics,Fibroblast Growth Factor 8: metabolism,Limb Buds,Limb Buds: physiology,Mice,Mice, Knockout,Retinal Dehydrogenase,Signal Transduction,Signal Transduction: physiology,Tretinoin,Tretinoin: pharmacology},
 pages = {1050-7},
 volume = {19},
 websites = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2701469&tool=pmcentrez&rendertype=abstract},
 month = {7},
 publisher = {Elsevier Ltd},
 day = {23},
 id = {515e0bca-299c-394e-b95d-ed7a2b842bc8},
 created = {2016-04-08T12:19:45.000Z},
 accessed = {2014-03-31},
 file_attached = {true},
 profile_id = {994bc413-6766-31df-917a-32165aa30f6c},
 group_id = {cec5aa9e-65e1-3c21-bc44-78fa6504020e},
 last_modified = {2017-03-14T10:42:46.538Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Zhao2009},
 folder_uuids = {37786225-e8d4-483b-be04-dfc97f200748},
 private_publication = {false},
 abstract = {Retinoic acid (RA) is thought to be a key signaling molecule involved in limb bud patterning along the proximodistal or anteroposterior axes functioning through induction of Meis2 and Shh, respectively. Here, we utilize Raldh2-/- and Raldh3-/- mouse embryos lacking RA synthesis to demonstrate that RA signaling is not required for limb expression of Shh and Meis2. We demonstrate that RA action is required outside of the limb field in the body axis during forelimb induction but that RA is unnecessary at later stages when hindlimb budding and patterning occur. We provide evidence for a model of trunk mesodermal RA action in which forelimb induction requires RA repression of Fgf8 in the developing trunk similar to how RA controls somitogenesis and heart development. We demonstrate that pectoral fin development in RA-deficient zebrafish embryos can be rescued by an FGF receptor antagonist SU5402. In addition, embryo ChIP assays demonstrate that RA receptors bind the Fgf8 promoter in vivo. Our findings suggest that RA signaling is not required for limb proximodistal or anteroposterior patterning but that RA inhibition of FGF8 signaling during the early stages of body axis extension provides an environment permissive for induction of forelimb buds.},
 bibtype = {article},
 author = {Zhao, Xianling and Sirbu, Ioan Ovidiu and Mic, Felix a and Molotkova, Natalia and Molotkov, Andrei and Kumar, Sandeep and Duester, Gregg},
 journal = {Current biology : CB},
 number = {12}
}

@article{
 title = {Spike inference from calcium imaging using sequential Monte Carlo methods.},
 type = {article},
 year = {2009},
 identifiers = {[object Object]},
 keywords = {animals,biological,calcium,calcium metabolism,cytology/metabolism,fluorescence,inbred c57bl,intracellular space,intracellular space metabolism,metabolism,mice,models,monte carlo method,neurons,neurons cytology,neurons metabolism,probability,time factors},
 pages = {636-655},
 volume = {97},
 websites = {http://dx.doi.org/10.1016/j.bpj.2008.08.005},
 month = {7},
 institution = {Department of Neuroscience, The Johns Hopkins School of Medicine, Baltimore, Maryland, USA. joshuav@jhu.edu},
 id = {ea71e181-8857-33ea-b063-d3d46eb47138},
 created = {2015-06-19T07:45:09.000Z},
 file_attached = {false},
 profile_id = {182bbbf9-24a3-3af3-9ed6-563e8f89259b},
 group_id = {8d229673-0aec-3014-b0f6-eda47f83e147},
 last_modified = {2015-06-19T07:45:23.000Z},
 read = {false},
 starred = {false},
 authored = {true},
 confirmed = {true},
 hidden = {false},
 citation_key = {smc-oopsi},
 source_type = {article},
 abstract = {As recent advances in calcium sensing technologies facilitate simultaneously imaging action potentials in neuronal populations, complementary analytical tools must also be developed to maximize the utility of this experimental paradigm. Although the observations here are fluorescence movies, the signals of interest--spike trains and/or time varying intracellular calcium concentrations--are hidden. Inferring these hidden signals is often problematic due to noise, nonlinearities, slow imaging rate, and unknown biophysical parameters. We overcome these difficulties by developing sequential Monte Carlo methods (particle filters) based on biophysical models of spiking, calcium dynamics, and fluorescence. We show that even in simple cases, the particle filters outperform the optimal linear (i.e., Wiener) filter, both by obtaining better estimates and by providing error bars. We then relax a number of our model assumptions to incorporate nonlinear saturation of the fluorescence signal, as well external stimulus and spike history dependence (e.g., refractoriness) of the spike trains. Using both simulations and in vitro fluorescence observations, we demonstrate temporal superresolution by inferring when within a frame each spike occurs. Furthermore, the model parameters may be estimated using expectation maximization with only a very limited amount of data (e.g., approximately 5-10 s or 5-40 spikes), without the requirement of any simultaneous electrophysiology or imaging experiments.},
 bibtype = {article},
 author = {Vogelstein, Joshua T. and Watson, Brendon O and Packer, Adam M and Yuste, Rafael and Jedynak, Bruno M and Paninski, Liam},
 journal = {Biophysical Journal},
 number = {2}
}

Paper  Website  abstract   bibtex   

@article{
 title = {Ectopic Meis1 expression in the mouse limb bud alters P-D patterning in a Pbx1-independent manner.},
 type = {article},
 year = {2009},
 identifiers = {[object Object]},
 keywords = {Animals,Body Patterning,Body Patterning: genetics,Body Patterning: physiology,Embryo, Mammalian,Embryo, Mammalian: embryology,Embryo, Mammalian: metabolism,Gene Expression Regulation, Developmental,Homeodomain Proteins,Homeodomain Proteins: genetics,Homeodomain Proteins: metabolism,Homeodomain Proteins: physiology,Immunohistochemistry,In Situ Hybridization,Limb Buds,Limb Buds: embryology,Limb Buds: metabolism,Mice,Mice, Inbred C57BL,Mice, Transgenic,Neoplasm Proteins,Neoplasm Proteins: genetics,Neoplasm Proteins: metabolism,Neoplasm Proteins: physiology,Time Factors,Transcription Factors,Transcription Factors: genetics,Transcription Factors: metabolism,Transcription Factors: physiology},
 pages = {1483-94},
 volume = {53},
 websites = {http://www.ncbi.nlm.nih.gov/pubmed/19247936},
 month = {1},
 id = {126d963a-2456-3fa6-94ca-b4f994d865d7},
 created = {2016-04-08T12:19:35.000Z},
 accessed = {2014-01-20},
 file_attached = {true},
 profile_id = {994bc413-6766-31df-917a-32165aa30f6c},
 group_id = {cec5aa9e-65e1-3c21-bc44-78fa6504020e},
 last_modified = {2017-03-14T10:42:46.538Z},
 read = {true},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Mercader2009},
 folder_uuids = {37786225-e8d4-483b-be04-dfc97f200748},
 private_publication = {false},
 abstract = {During limb development, expression of the TALE homeobox transcription factor Meis1 is activated by retinoic acid in the proximal-most limb bud regions, which give rise to the upper forelimb and hindlimb. Early subdivision of the limb bud into proximal Meis-positive and distal Meis-negative domains is necessary for correct proximo-distal (P-D) limb development in the chick, since ectopic Meis1 overexpression abolishes distal limb structures, produces a proximal shift of limb identities along the P-D axis, and proximalizes distal limb cell affinity properties. To determine whether Meis activity is also required for P-D limb specification in mammals, we generated transgenic mice ectopically expressing Meis1 in the distal limb mesenchyme under the control of the Msx2 promoter. Msx2:Meis1 transgenic mice display altered P-D patterning and shifted P-D Hox gene expression domains, similar to those previously described for the chicken. Meis proteins function in cooperation with PBX factors, another TALE homeodomain subfamily. Meis-Pbx interaction is required for nuclear localization of both proteins in cell culture, and is important for their DNA-binding and transactivation efficiency. During limb development, Pbx1 nuclear expression correlates with the Meis expression domain, and Pbx1 has been proposed as the main Meis partner in this context; however, we found that Pbx1 deficiency did not modify the limb phenotype of Msx2:Meis1 mice. Our results indicate a conserved role of Meis activity in P-D specification of the tetrapod limb and suggest that Pbx function in this context is either not required or is provided by partners other than Pbx1.},
 bibtype = {article},
 author = {Mercader, Nadia and Selleri, Licia and Criado, Luis Miguel and Pallares, Pilar and Parras, Carlos and Cleary, Michael L and Torres, Miguel},
 journal = {The International journal of developmental biology},
 number = {8-10}
}

Paper  doi  bibtex   

@article{Tang2009,
	title = {Faithful expression of multiple proteins via {2A}-peptide self-processing: a versatile and reliable method for manipulating brain circuits.},
	volume = {29},
	issn = {1529-2401},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/19587267},
	doi = {10.1523/JNEUROSCI.0359-09.2009},
	number = {27},
	urldate = {2013-08-09},
	journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	author = {Tang, Wannan and Ehrlich, Ingrid and Wolff, Steffen B E and Michalski, Ann-Marie and Wölfl, Stefan and Hasan, Mazahir T and Lüthi, Andreas and Sprengel, Rolf},
	month = jul,
	year = {2009},
	pmid = {19587267},
	keywords = {\#nosource, Amino Acid Sequence, Animals, Archaeal Proteins, Archaeal Proteins: biosynthesis, Archaeal Proteins: genetics, Archaeal Proteins: metabolism, Cell Line, Cells, Cultured, Cytomegalovirus, Cytomegalovirus: chemistry, Cytomegalovirus: genetics, Dependovirus, Dependovirus: chemistry, Dependovirus: genetics, Gene Expression Regulation, Bacterial, Gene Expression Regulation, Bacterial: physiology, Gene Expression Regulation, Viral, Gene Expression Regulation, Viral: physiology, Hippocampus, Hippocampus: metabolism, Hippocampus: microbiology, Hippocampus: physiology, Hippocampus: virology, Humans, Mice, Molecular Sequence Data, Nerve Net, Nerve Net: metabolism, Nerve Net: microbiology, Nerve Net: physiology, Nerve Net: virology, Nerve Tissue Proteins, Nerve Tissue Proteins: biosynthesis, Nerve Tissue Proteins: genetics, Nerve Tissue Proteins: metabolism, Neurons, Neurons: metabolism, Neurons: microbiology, Neurons: virology, Protein Processing, Post-Translational, Protein Processing, Post-Translational: genetics, Rats, Viral Proteins, Viral Proteins: biosynthesis, Viral Proteins: genetics, Viral Proteins: metabolism},
	pages = {8621--9},
}

Paper  doi  abstract   bibtex   

@article{Nimmerjahn2009,
	title = {Motor behavior activates {Bergmann} glial networks.},
	volume = {62},
	issn = {1097-4199},
	url = {http://linkinghub.elsevier.com/retrieve/pii/S089662730900244X},
	doi = {10.1016/j.neuron.2009.03.019},
	abstract = {Although it is firmly established that neuronal activity is a prime determinant of animal behavior, relationships between astrocytic excitation and animal behavior have remained opaque. Cerebellar Bergmann glia are radial astrocytes that are implicated in motor behavior and exhibit Ca(2+) excitation. However, Ca(2+) excitation in these cells has not previously been studied in behaving animals. Using two-photon microscopy we found that Bergmann glia exhibit three forms of Ca(2+) excitation in awake, behaving mice. Two of these are ongoing within the cerebellar vermis. During locomotor performance concerted Ca(2+) excitation arises in networks of at least hundreds of Bergmann glia extending across several hundred microns or more. Concerted Ca(2+) excitation was abolished by anesthesia or blockade of either neural activity or glutamatergic transmission. Thus, large networks of Bergmann glia can be activated by specific animal behaviors and undergo excitation of sufficient magnitude to potentially initiate macroscopic changes in brain dynamics or blood flow.},
	number = {3},
	urldate = {2012-07-31},
	journal = {Neuron},
	author = {Nimmerjahn, Axel and Mukamel, Eran A. and Schnitzer, Mark J.},
	month = may,
	year = {2009},
	pmid = {19447095},
	note = {Publisher: Elsevier Ltd
ISBN: 0896-6273},
	keywords = {Animals, Astrocytes, Astrocytes: physiology, CELLBIO, Calcium Signaling, Calcium Signaling: physiology, Cell Communication, Cell Communication: physiology, Cerebellum, Cerebellum: cytology, Cerebellum: physiology, Inbred C57BL, MOLNEURO, Male, Membrane Potentials, Membrane Potentials: physiology, Mice, Motor Activity, Motor Activity: physiology, Motor Skills, Motor Skills: physiology, SYSNEURO, glia},
	pages = {400--12},
}

Paper  doi  abstract   bibtex   

@article{tabone-eglinger_kit_2008,
	title = {{KIT} mutations induce intracellular retention and activation of an immature form of the {KIT} protein in gastrointestinal stromal tumors},
	volume = {14},
	issn = {1078-0432 (PRINT) 1078-0432 (LINKING)},
	url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18413817},
	doi = {14/8/2285 [pii] 10.1158/1078-0432.CCR-07-4102},
	abstract = {PURPOSE: Gastrointestinal stromal tumors (GIST) are frequently associated with gain-of-function mutations of KIT, which can be inhibited by imatinib both in vitro and in vivo. The survival of patients with GIST, following imatinib therapy, has been correlated with the nature of mutations but not with KIT expression. EXPERIMENTAL DESIGN: Subcellular localization, activation, and trafficking of the mature and the immature forms of KIT were investigated in GIST samples and in NIH3T3 cells infected with two different GIST-type exon 11-mutated human KIT cDNA. RESULTS: Paranuclear dot expression of KIT was more frequent in GISTs with homozygous KIT mutations than in those with heterozygous (P = 0.01) or no mutations (P {\textless} 0.01). Activation of the immature 125 kDa form of KIT was detected in most GISTs with KIT mutations but not in GISTs without KIT mutations. In NIH3T3 cells, mutant KIT was mainly retained within endoplasmic reticulum and Golgi compartments in an immature constitutively phosphorylated form, whereas the wild-type KIT was expressed at the plasma membrane, in a mature nonphosphorylated form. Imatinib-induced inhibition of the phosphorylation of immature and mature mutant KIT proteins resulted in the restoration of KIT expression at the cell surface. CONCLUSIONS: These results show that GIST-type KIT mutations induce an activation-dependent alteration of normal maturation and trafficking, resulting in the intracellular retention of the activated kinase within the cell. These observations likely account for the absence of correlation between response to imatinib and KIT expression using immunohistochemistry and may deserve to be investigated in other tyrosine kinase-activated tumors.},
	number = {8},
	journal = {Clin Cancer Res},
	author = {Tabone-Eglinger, S. and Subra, F. and El Sayadi, H. and Alberti, L. and Tabone, E. and Michot, J. P. and Theou-Anton, N. and Lemoine, A. and Blay, J. Y. and Emile, J. F.},
	year = {2008},
	keywords = {*Mutation, 3T3, Animals, Cell, Cells, Factor/pharmacology, Gastrointestinal, Humans, Mice, NIH, Phosphorylation, Proteins, Proto-Oncogene, Stem, Stromal, Tumors/genetics/*metabolism, c-kit/*genetics/*metabolism},
	pages = {2285--94},
}

Website  abstract   bibtex   

@article{
 title = {Clonogenic multiple myeloma progenitors, stem cell properties, and drug resistance.},
 type = {article},
 year = {2008},
 identifiers = {[object Object]},
 keywords = {Animals,Antigens,Antineoplastic Agents,Antineoplastic Agents: pharmacology,B-Lymphocytes,B-Lymphocytes: pathology,Boronic Acids,Boronic Acids: pharmacology,CD20,CD20: analysis,CD27,CD27: analysis,Clone Cells,Clone Cells: drug effects,Clone Cells: pathology,Cyclophosphamide,Cyclophosphamide: analogs & derivatives,Cyclophosphamide: pharmacology,Dexamethasone,Dexamethasone: pharmacology,Drug Resistance,Humans,Inbred Strains,Mice,Multiple Myeloma,Multiple Myeloma: pathology,Neoplasm,Neoplastic Stem Cells,Neoplastic Stem Cells: drug effects,Neoplastic Stem Cells: pathology,Plasma Cells,Plasma Cells: drug effects,Plasma Cells: pathology,Pyrazines,Pyrazines: pharmacology,Syndecan-1,Syndecan-1: analysis,Thalidomide,Thalidomide: analogs & derivatives,Thalidomide: pharmacology,Tumor Stem Cell Assay},
 pages = {190-7},
 volume = {68},
 websites = {http://cancerres.aacrjournals.org/content/68/1/190.full},
 month = {1},
 day = {1},
 id = {494ed8c9-5c08-3403-8b42-0d004f92312a},
 created = {2016-06-24T20:49:19.000Z},
 accessed = {2014-11-18},
 file_attached = {false},
 profile_id = {954a987f-819f-3985-95a4-2991e0cf0552},
 group_id = {8440dcff-74cc-3783-aef7-fe2749cfc7ef},
 last_modified = {2016-06-24T20:49:19.000Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Matsui2008},
 abstract = {Many agents are active in multiple myeloma, but the majority of patients relapse. This clinical pattern suggests most cancer cells are eliminated, but cells with the clonogenic potential to mediate tumor regrowth are relatively chemoresistant. Our previous data suggested that CD138(+) multiple myeloma plasma cells cannot undergo long-term proliferation but rather arise from clonogenic CD138(neg) B cells. We compared the relative sensitivity of these distinct cell types to clinical antimyeloma agents and found that dexamethasone, lenadilomide, bortezomib, and 4-hydroxycyclophosphamide inhibited CD138(+) multiple myeloma plasma cells but had little effect on CD138(neg) precursors in vitro. We further characterized clonogenic multiple myeloma cells and stained cell lines using the Hoechst side population and Aldefluor assays. Each assay identified CD138(neg) cells suggesting that they possess high drug efflux capacity and intracellular drug detoxification activity. We also found that multiple myeloma cells expressing the memory B-cell markers CD20 and CD27 could give rise to clonogenic multiple myeloma growth in vitro and engraft immunodeficient nonobese diabetes/severe combined immunodeficient mice during both primary and secondary transplantation. Furthermore, both the side population and Aldefluor assays were capable of identifying circulating clonotypic memory B-cell populations within the peripheral blood of multiple myeloma patients. Our results suggest that circulating clonotypic B-cell populations represent multiple myeloma stem cells, and the relative drug resistance of these cells is mediated by processes that protect normal stem cells from toxic injury.},
 bibtype = {article},
 author = {Matsui, William and Wang, Qiuju and Barber, James P and Brennan, Sarah and Smith, B Douglas and Borrello, Ivan and McNiece, Ian and Lin, Lan and Ambinder, Richard F and Peacock, Craig and Watkins, D Neil and Huff, Carol Ann and Jones, Richard J},
 journal = {Cancer research},
 number = {1}
}

Website  abstract   bibtex   

@article{
 title = {Visualizing cold spots: TRPM8-expressing sensory neurons and their projections.},
 type = {article},
 year = {2008},
 identifiers = {[object Object]},
 keywords = {Afferent Pathways,Afferent Pathways: metabolism,Animals,Antipruritics,Antipruritics: pharmacology,Blood Vessels,Blood Vessels: innervation,Blood Vessels: metabolism,Calcitonin Gene-Related Peptide,Calcitonin Gene-Related Peptide: metabolism,Capsaicin,Capsaicin: pharmacology,Cells, Cultured,Cold Temperature,Ganglia, Spinal,Ganglia, Spinal: cytology,Gene Expression Regulation,Gene Expression Regulation: drug effects,Gene Expression Regulation: physiology,Green Fluorescent Proteins,Green Fluorescent Proteins: genetics,Green Fluorescent Proteins: metabolism,Menthol,Menthol: pharmacology,Mice,Mice, Inbred C57BL,Mice, Transgenic,Neurons, Afferent,Neurons, Afferent: cytology,Neurons, Afferent: drug effects,Neurons, Afferent: physiology,Spinal Cord,Spinal Cord: cytology,Spinal Cord: physiology,TRPM Cation Channels,TRPM Cation Channels: deficiency,TRPM Cation Channels: metabolism,TRPV Cation Channels,TRPV Cation Channels: metabolism},
 pages = {566-75},
 volume = {28},
 websites = {http://www.jneurosci.org/content/28/3/566.long},
 month = {1},
 day = {16},
 id = {4d21c71d-9f99-3b94-b72a-2b06dbb03877},
 created = {2016-02-10T11:58:54.000Z},
 accessed = {2016-02-10},
 file_attached = {false},
 profile_id = {3e449d8a-90c5-35f9-aaa3-cdbb3ca120e9},
 group_id = {2ad31c26-29a3-3f9c-b495-1b90dc1c4bb6},
 last_modified = {2016-02-10T11:58:54.000Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 abstract = {Environmental stimuli such as temperature and pressure are sensed by dorsal root ganglion (DRG) neurons. DRG neurons are heterogeneous, but molecular markers that identify unique functional subpopulations are mainly lacking. ThermoTRPs are members of the transient receptor potential family of ion channels and are gated by shifts in temperature. TRPM8 is activated by cooling, and TRPM8-deficient mice have severe deficits in cool thermosensation. The anatomical and functional properties of TRPM8-expressing fibers have not been not comprehensively investigated. We use mice engineered to express the farnesylated enhanced green fluorescent protein (EGFPf) from the TRPM8 locus (TRPM8(EGFPf)) to explore this issue. Virtually all EGFPf-positive cultured DRG neurons from hemizygous mice (TRPM8(EGFPf/+)) responded to cold and menthol. In contrast, EGFPf-positive DRGs from homozygous mice (TRPM8(EGFPf/EGFPf)) had drastically reduced cold responses and no menthol responses. In vivo, EGFPf-positive neurons marked a unique population of DRG neurons, a majority of which do not coexpress nociceptive markers. The fraction of DRG neurons expressing EGFPf was not altered under an inflammatory condition, although an increase in TRPV1-coexpressing neurons was observed. TRPM8(EGFPf) neurons project to the superficial layer I of the spinal cord, making distinct contacts when compared with peptidergic projections. At the periphery, TRPM8(EGFPf) projections mark unique endings in the most superficial layers of epidermis, including bush/cluster endings of the mystacial pads. We show that TRPM8 expression functionally associates with cold sensitivity in cultured DRGs, and provide the first glimpses of the unique anatomical architecture of cold fibers in vivo.},
 bibtype = {article},
 author = {Dhaka, Ajay and Earley, Taryn J and Watson, James and Patapoutian, Ardem},
 journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
 number = {3}
}

@article{weiler_top-down_2008,
	title = {Top-down laminar organization of the excitatory network in motor cortex},
	volume = {11},
	issn = {1097-6256},
	doi = {10.1038/nn2049},
	abstract = {Cortical layering is a hallmark of the mammalian neocortex and a major determinant of local synaptic circuit organization in sensory systems. In motor cortex, the laminar organization of cortical circuits has not been resolved, although their input-output operations are crucial for motor control. Here, we developed a general approach for estimating layer-specific connectivity in cortical circuits and applied it to mouse motor cortex. From these data we computed a laminar presynaptic --{\textgreater} postsynaptic connectivity matrix, W(post,pre), revealing a complement of stereotypic pathways dominated by layer 2 outflow to deeper layers. Network modeling predicted, and experiments with disinhibited slices confirmed, that stimuli targeting upper, but not lower, cortical layers effectively evoked network-wide events. Thus, in motor cortex, descending excitation from a preamplifier-like network of upper-layer neurons drives output neurons in lower layers. Our analysis provides a quantitative wiring-diagram framework for further investigation of the excitatory networks mediating cortical mechanisms of motor control.},
	language = {eng},
	number = {3},
	journal = {Nature neuroscience},
	author = {Weiler, Nicholas and Wood, Lydia and Yu, Jianing and Solla, Sara A and Shepherd, Gordon M G},
	month = mar,
	year = {2008},
	pmid = {18246064},
	keywords = {Action Potentials, Animals, Brain Mapping, Excitatory Postsynaptic Potentials, Glutamic Acid, Mice, Motor Cortex, Nerve Net, Neural Networks (Computer), Neural Pathways, Neurons, Organ Culture Techniques, Photic Stimulation, Photochemistry, Synaptic Transmission},
	pages = {360--366}
}

Paper  doi  abstract   bibtex   

@article{Toni2008,
	title = {Neurons born in the adult dentate gyrus form functional synapses with target cells.},
	volume = {11},
	issn = {1546-1726},
	url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2572641&tool=pmcentrez&rendertype=abstract},
	doi = {10.1038/nn.2156},
	abstract = {Adult neurogenesis occurs in the hippocampus and the olfactory bulb of the mammalian CNS. Recent studies have demonstrated that newborn granule cells of the adult hippocampus are postsynaptic targets of excitatory and inhibitory neurons, but evidence of synapse formation by the axons of these cells is still lacking. By combining retroviral expression of green fluorescent protein in adult-born neurons of the mouse dentate gyrus with immuno-electron microscopy, we found output synapses that were formed by labeled terminals on appropriate target cells in the CA3 area and the hilus. Furthermore, retroviral expression of channelrhodopsin-2 allowed us to light-stimulate newborn granule cells and identify postsynaptic target neurons by whole-cell recordings in acute slices. Our structural and functional evidence indicates that axons of adult-born granule cells establish synapses with hilar interneurons, mossy cells and CA3 pyramidal cells and release glutamate as their main neurotransmitter.},
	number = {8},
	urldate = {2013-08-15},
	journal = {Nature neuroscience},
	author = {Toni, Nicolas and Laplagne, Diego a and Zhao, Chunmei and Lombardi, Gabriela and Ribak, Charles E and Gage, Fred H and Schinder, Alejandro F},
	month = aug,
	year = {2008},
	pmid = {18622400},
	keywords = {\#nosource, Action Potentials, Action Potentials: drug effects, Action Potentials: physiology, Action Potentials: radiation effects, Animals, Carrier Proteins, Carrier Proteins: biosynthesis, Carrier Proteins: genetics, Dentate Gyrus, Dentate Gyrus: cytology, Dentate Gyrus: metabolism, Dentate Gyrus: virology, Female, GABA Antagonists, GABA Antagonists: pharmacology, Gene Transfer Techniques, Genes, Reporter, Glutamic Acid, Glutamic Acid: metabolism, Humans, Interneurons, Interneurons: physiology, Interneurons: ultrastructure, Light, Luminescent Proteins, Luminescent Proteins: biosynthesis, Luminescent Proteins: genetics, Mice, Mice, Inbred C57BL, Moloney murine leukemia virus, Moloney murine leukemia virus: genetics, Mossy Fibers, Hippocampal, Mossy Fibers, Hippocampal: metabolism, Mossy Fibers, Hippocampal: ultrastructure, Mossy Fibers, Hippocampal: virology, Neurons, Neurons: drug effects, Neurons: physiology, Neurons: radiation effects, Organ Culture Techniques, Patch-Clamp Techniques, Photic Stimulation, Presynaptic Terminals, Presynaptic Terminals: physiology, Presynaptic Terminals: ultrastructure, Synapses, Synapses: genetics, Synapses: physiology, Synapses: ultrastructure, Synaptic Transmission, Synaptic Transmission: drug effects, Synaptic Transmission: physiology, Synaptic Transmission: radiation effects},
	pages = {901--7},
}

@article{liu_discovery_2008,
	title = {Discovery and characterization of novel tryptophan hydroxylase inhibitors that selectively inhibit serotonin synthesis in the gastrointestinal tract},
	volume = {325},
	issn = {1521-0103},
	doi = {10.1124/jpet.107.132670},
	abstract = {5-Hydroxytryptamine (serotonin) (5-HT) is a neurotransmitter with both central and peripheral functions, including the modulation of mood, appetite, hemodynamics, gastrointestinal (GI) sensation, secretion, and motility. Its synthesis is initiated by the enzyme tryptophan hydroxylase (TPH). Two isoforms of TPH have been discovered: TPH1, primarily expressed in the enterochromaffin cells of the gastrointestinal tract, and TPH2, expressed exclusively in neuronal cells. Mice lacking Tph1 contain little to no 5-HT in the blood and GI tract while maintaining normal levels in the brain. Because GI 5-HT is known to play important roles in normal and pathophysiology, we set out to discover and characterize novel compounds that selectively inhibit biosynthesis of GI 5-HT. Here, we describe two of a series of these inhibitors that are potent for TPH activity both in biochemical and cell-based assays. This class of compounds has unique properties with respect to pharmacokinetic and pharmacodynamic effects on GI serotonin production. Similar to the Tph1 knockout results, these TPH inhibitors have the ability to selectively reduce 5-HT levels in the murine GI tract without affecting brain 5-HT levels. In addition, administration of these compounds in a ferret model of chemotherapy-induced emesis caused modest reductions of intestinal serotonin levels and a decreased emetic response. These findings suggest that GI-specific TPH inhibitors may provide novel treatments for various gastrointestinal disorders associated with dysregulation of the GI serotonergic system, such as chemotherapy-induced emesis and irritable bowel syndrome.},
	language = {eng},
	number = {1},
	journal = {The Journal of Pharmacology and Experimental Therapeutics},
	author = {Liu, Qingyun and Yang, Qi and Sun, Weimei and Vogel, Pete and Heydorn, William and Yu, Xiang-Qing and Hu, Zhixiang and Yu, Wangsheng and Jonas, Brandie and Pineda, Randy and Calderon-Gay, Valerie and Germann, Michael and O'Neill, Emily and Brommage, Robert and Cullinan, Emily and Platt, Ken and Wilson, Alan and Powell, Dave and Sands, Arthur and Zambrowicz, Brian and Shi, Zhi-Cai},
	month = apr,
	year = {2008},
	pmid = {18192499},
	keywords = {Animals, Brain Chemistry, Ferrets, Gastrointestinal Tract, Irritable Bowel Syndrome, Mice, Mice, Knockout, Serotonin, Tryptophan Hydroxylase, Vomiting},
	pages = {47--55},
}

Paper  doi  abstract   bibtex   

@article{ bourin_animal_2007,
  title = {Animal models of anxiety in mice},
  volume = {21},
  issn = {1472-8206},
  url = {http://onlinelibrary.wiley.com/doi/10.1111/j.1472-8206.2007.00526.x/abstract},
  doi = {10.1111/j.1472-8206.2007.00526.x},
  abstract = {Among the multiple possibilities to study human pathologies, animal models remain one of the most used pathways. They allow to access to unavailable answers in human patients and to learn about mechanisms of action of drugs. Primarily developed with rats, animal models in anxiety have been adapted with a mixed success for mice, an easy-to-use mammal with better genetic possibilities than rats. In this review, we have focused on the most used animal models in anxiety in mice. Both conditioned and unconditioned models are described, to represent all types of animal models of anxiety. Behavioural studies require strong care for variable parameters, linked to environment, handling or paradigm; we have discussed about this topic. Finally, we focused on the consequences of re-exposure to the apparatus. Test–retest procedures can bring in new answers, but should be deeply studied, to revalidate the whole paradigm as an animal model of anxiety.},
  language = {en},
  number = {6},
  urldate = {2013-09-23TZ},
  journal = {Fundamental \& Clinical Pharmacology},
  author = {Bourin, Michel and Petit-Demoulière, Benoit and Nic Dhonnchadha, Brid and Hascöet, Martine},
  year = {2007},
  keywords = {Anxiety, Mice, animal model, behavioural studies, test–retest},
  pages = {567--574}
}

Paper  doi  abstract   bibtex   

@article{Newman2007,
	title = {Alzheimer disease: amyloidogenesis, the presenilins and animal models.},
	volume = {1772},
	issn = {0006-3002},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/17208417},
	doi = {10.1016/j.bbadis.2006.12.001},
	abstract = {Alzheimer's disease is the most prevalent form of dementia. Neuropathogenesis is proposed to be a result of the accumulation of amyloid beta peptides in the brain together with oxidative stress mechanisms and neuroinflammation. The presenilin proteins are central to the gamma-secretase cleavage of the amyloid prescursor protein (APP), releasing the amyloid beta peptide. Point mutations in the presenilin genes lead to cases of familial Alzheimer's disease by increasing APP cleavage resulting in excess amyloid beta formation. This review discusses the molecular mechanism of Alzheimer's disease with a focus on the presenilin genes. Alternative splicing of transcripts from these genes and how these may function in several disease states is discussed. There is an emphasis on the importance of animal models in elucidating the molecular mechanisms behind the development of Alzheimer's disease and how the zebrafish, Danio rerio, can be used as a model organism for analysis of presenilin function and Alzheimer's disease pathogenesis.},
	number = {3},
	urldate = {2014-03-31},
	journal = {Biochimica et biophysica acta},
	author = {Newman, M and Musgrave, I F and Musgrave, F I and Lardelli, M},
	month = mar,
	year = {2007},
	pmid = {17208417},
	keywords = {Alzheimer Disease, Alzheimer Disease: etiology, Alzheimer Disease: genetics, Amyloid beta-Protein Precursor, Amyloid beta-Protein Precursor: metabolism, Animals, Disease Models, Animal, Mice, Point Mutation, Presenilins, Presenilins: metabolism, Zebrafish, Zebrafish: genetics, Zebrafish: metabolism},
	pages = {285--97},
}

@article{ sibille_lack_2007,
  title = {Lack of serotonin1B receptor expression leads to age-related motor dysfunction, early onset of brain molecular aging and reduced longevity},
  volume = {12},
  issn = {1359-4184},
  doi = {10.1038/sj.mp.4001990},
  abstract = {Normal aging of the brain differs from pathological conditions and is associated with increased risk for psychiatric and neurological disorders. In addition to its role in the etiology and treatment of mood disorders, altered serotonin (5-{HT}) signaling is considered a contributing factor to aging; however, no causative role has been identified in aging. We hypothesized that a deregulation of the 5-{HT} system would reveal its contribution to age-related processes and investigated behavioral and molecular changes throughout adult life in mice lacking the regulatory presynaptic 5-{HT}(1B) receptor (5-{HT}(1B)R), a candidate gene for 5-{HT}-mediated age-related functions. We show that the lack of 5-{HT}(1B)R (Htr1b({KO}) mice) induced an early age-related motor decline and resulted in decreased longevity. Analysis of life-long transcriptome changes revealed an early and global shift of the gene expression signature of aging in the brain of Htr1b({KO}) mice. Moreover, molecular changes reached an apparent maximum effect at 18-months in Htr1b({KO}) mice, corresponding to the onset of early death in that group. A comparative analysis with our previous characterization of aging in the human brain revealed a phylogenetic conservation of age-effect from mice to humans, and confirmed the early onset of molecular aging in Htr1b({KO}) mice. Potential mechanisms appear independent of known central mechanisms (Bdnf, inflammation), but may include interactions with previously identified age-related systems ({IGF}-1, sirtuins). In summary, our findings suggest that the onset of age-related events can be influenced by altered 5-{HT} function, thus identifying 5-{HT} as a modulator of brain aging, and suggesting age-related consequences to chronic manipulation of 5-{HT}.},
  language = {eng},
  number = {11},
  journal = {Molecular Psychiatry},
  author = {Sibille, E. and Su, J. and Leman, S. and Le Guisquet, A. M. and Ibarguen-Vargas, Y. and Joeyen-Waldorf, J. and Glorioso, C. and Tseng, G. C. and Pezzone, M. and Hen, R. and Belzung, C.},
  month = {November},
  year = {2007},
  pmid = {17420766},
  pmcid = {PMC2515886},
  keywords = {Age Factors, Aging, Analysis of Variance, Animals, Animals, Newborn, Behavior, Animal, Dopamine Plasma Membrane Transport Proteins, Enzyme-Linked Immunosorbent Assay, Gene Expression, Gene Expression Regulation, Hand Strength, In Situ Hybridization, Maze Learning, Mice, Mice, Knockout, Microarray Analysis, Motor Activity, Reaction Time, Receptor, Serotonin, 5-{HT}1B, Survival Analysis},
  pages = {1042--1056, 975}
}

@article{zeskind_nucleic_2007,
	title = {Nucleic acid and protein mass mapping by live-cell deep-ultraviolet microscopy},
	volume = {4},
	number = {7},
	journal = {Nature Methods},
	author = {Zeskind, Benjamin J and Jordan, Caroline D and Timp, Winston and Trapani, Linda and Waller, Guichy and Horodincu, Victor and Ehrlich, Daniel J and Matsudaira, Paul},
    author+an = {3=pi},
	month = jul,
	year = {2007},
	keywords = {Animals, Cell Movement, Computer-Assisted, Humans, Image Processing, Mice, Microscopy, Mitosis, Nucleic Acids, Nucleic Acids: analysis, Nucleic Acids: metabolism, Proteins, Proteins: analysis, Proteins: metabolism, Ultraviolet, Ultraviolet: methods},
	pages = {567--9}
}

@Article{VonWegner_2007_5301,
  author = {Von Wegner, F. and Both, M. and Fink, R. H. and Friedrich, O.},
 journal = {IEEE Transactions on Medical Imaging},
 number = {7},
 pages = {925-34},
 title = {Fast XYT imaging of elementary calcium release events in muscle with multifocal multiphoton microscopy and wavelet denoising and detection},
 volume = {26},
 year = {2007},
 keywords = {Algorithms, Animals, Calcium/*metabolism, Calcium, Signaling/physiology, Cells, Cultured, Image, Enhancement/methods, Image, Interpretation, Computer-Assisted/*methods, Imaging, Three-Dimensional/methods, Metabolic, Clearance, Rate, Mice, Microscopy, Fluorescence, Multiphoton/*methods, Muscle, Fibers/*cytology/*metabolism, Muscle, Skeletal/*cytology/*metabolism, Reproducibility, of, Results, Sensitivity, and, Specificity},
 title_with_no_special_chars = {Fast XYT imaging of elementary calcium release events in muscle with multifocal multiphoton microscopy and wavelet denoising and detection}
}

Paper  doi  abstract   bibtex   

@article{viberg_neonatal_2006,
	title = {Neonatal exposure to higher brominated diphenyl ethers, hepta-, octa-, or nonabromodiphenyl ether, impairs spontaneous behavior and learning and memory functions of adult mice.},
	volume = {92},
	issn = {1096-6080},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/16611620},
	doi = {10.1093/toxsci/kfj196},
	abstract = {Polybrominated diphenyl ethers (PBDEs), used as flame retardants, have been shown to be increasing in the environment and in human mother's milk. We have earlier reported that lower brominated PBDEs, such as tetra-, penta-, and hexa-brominated diphenyl ethers, can cause developmental neurotoxic effects in mice. Recently, this was also observed with the full-brominated PBDE, deca-brominated diphenyl ether (PBDE 209), although it was suggested that the effects were caused by a (possibly debrominated) metabolite thereof. The present study revealed that 2,2',3,3',4,4',5,5',6-nonabromodiphenyl ether (PBDE 206), 2,2',3,4,4',5,5',6-octabromodiphenyl ether (PBDE 203), and to a minor extent also 2,2',3,4,4',5',6'-heptabromodiphenyl ether (PBDE 183) can induce developmental neurotoxic effects. Neonatal Naval Medical Research Institute male mice were exposed on postnatal day 3 or 10 to PBDE 206, PBDE 203, or PBDE 183, given as a single oral dose of 21 mumol/kg body weight. At the adult age of 2-3 months, the mice were observed for performance in a spontaneous behavior test and the Morris water maze test. PBDE 203 and PBDE 206, when administered on neonatal day 10, caused disturbances in spontaneous behavior, leading to disrupted habituation and a hyperactive condition in adults at the age of 2 months. These behavioral changes were also seen in 2-month-old mice exposed to PBDE 203 on neonatal day 3. Furthermore, exposure to PBDE 203 on neonatal day 10 affected learning and memory functions in adult mice. The developmental neurotoxic effects were most pronounced in mice exposed to PBDE 203. These developmental neurobehavioral defects were in agreement with those we observed previously with lower brominated PBDEs and with PBDE 209. It is important to consider the fact that different PBDE congeners can have differing degrees of potency, when comparing levels of PBDEs in the environment and in mother's milk.},
	number = {1},
	journal = {Toxicological sciences},
	author = {Viberg, Henrik and Johansson, Niclas and Fredriksson, Anders and Eriksson, Johan and Marsh, Göran and Eriksson, Per},
	month = jul,
	year = {2006},
	pmid = {16611620},
	keywords = {Animal, Animal: drug effects, Animals, Behavior, Ethers, Flame retardants, Learning, Learning: drug effects, Male, Memory, Memory: drug effects, Mice, Newborn, Polybrominated Biphenyls, Polybrominated Biphenyls: toxicity, frelec, tox},
	pages = {211--8},
}

@article{el_messaoudi_coactivator-associated_2006,
	title = {Coactivator-associated arginine methyltransferase 1 ({CARM}1) is a positive regulator of the {Cyclin} {E}1 gene.},
	volume = {103},
	issn = {0027-8424},
	doi = {10.1073/pnas.0605692103},
	abstract = {The Cyclin E1 gene (CCNE1) is an ideal model to explore the mechanisms that control the transcription of cell cycle-regulated genes whose expression rises transiently before entry into S phase. E2F-dependent regulation of the CCNE1 promoter was shown to correlate with changes in the level of H3-K9 acetylation/methylation of nucleosomal histones positioned at the transcriptional start site region. Here we show that, upon growth stimulation, the same region is subject to variations of H3-R17 and H3-R26 methylation that correlate with the recruitment of coactivator-associated arginine methyltransferase 1 (CARM1) onto the CCNE1 and DHFR promoters. Accordingly, CARM1-deficient cells lack these modifications and present lowered levels and altered kinetics of CCNE1 and DHFR mRNA expression. Consistently, reporter gene assays demonstrate that CARM1 functions as a transcriptional coactivator for their E2F1/DP1-stimulated expression. CARM1 recruitment at the CCNE1 gene requires activator E2Fs and ACTR, a member of the p160 coactivator family that is frequently overexpressed in human breast cancer. Finally, we show that grade-3 breast tumors present coelevated mRNA levels of ACTR and CARM1, along with their transcriptional target CCNE1. All together, our results indicate that CARM1 is an important regulator of the CCNE1 gene.},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	author = {El Messaoudi, Selma and Fabbrizio, Eric and Rodriguez, Carmen and Chuchana, Paul and Fauquier, Lucas and Cheng, Donghang and Theillet, Charles and Vandel, Laurence and Bedford, Mark T and Sardet, Claude and Messaoudi, Selma El and Fabbrizio, Eric and Rodriguez, Carmen and Chuchana, Paul and Fauquier, Lucas and Cheng, Donghang and Theillet, Charles and Vandel, Laurence and Bedford, Mark T and Sardet, Claude},
	year = {2006},
	pmid = {16938873},
	keywords = {Activin Receptors- Type I, Animals, Cell Culture Techniques, Cell Proliferation, Cells- Cultured, E2F Transcription Factors, Fibroblasts, Gene Expression Regulation, Genes- Reporter, Genes- cdc, Histones, Kinetics, Luciferases, Methylation, Mice, MicroRNAs, NIH 3T3 Cells, Nucleosomes, Promoter Regions- Genetic, Protein-Arginine N-Methyltransferases, RNA- Messenger, RNA- Small Interfering, Swiss 3T3 Cells, Trans-Activators, Transcription Factor DP1},
	pages = {13351--13356}
}

Paper  doi  abstract   bibtex   

@article{Biddinger-2006-ID14,
  title     = {Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of
               insulin and sterol regulatory element-binding protein-1c.},
  abstract  = {Stearoyl-CoA desaturase ({SCD})1 catalyzes the rate-limiting reaction of
               monounsaturated fatty acid ({MUFA}) synthesis and plays an important role
               in the development of obesity. {SCD}1 is suppressed by leptin but induced
               by insulin. We have used animal models to dissect the effects of these
               hormones on {SCD}1. In the first model, leptin-deficient ob/ob mice were
               treated with either leptin alone or with both leptin and insulin to prevent
               the leptin-mediated fall in insulin. In the second model, mice with a
               liver-specific knockout of the insulin receptor ({LIRKO}) and their
               littermate controls ({LOX}s) were treated with leptin. As expected, leptin
               decreased {SCD}1 transcript, protein, and activity by >60\% in ob/ob and
               {LOX} mice. However, the effects of leptin were not diminished by the
               continued presence of hyperinsulinemia in ob/ob mice treated with both
               leptin and insulin or the absence of insulin signaling in {LIRKO} mice.
               Furthermore, genetic knockout of sterol regulatory element-binding protein
               ({SREBP})-1c, the lipogenic transcription factor that mediates the effects
               of insulin on {SCD}1, also had no effect on the ability of leptin to
               decrease either {SCD}1 transcript or activity. Thus, the effect of leptin
               on {SCD}1 in liver is independent of insulin and {SREBP}-1c, and leptin,
               rather than insulin, is the major regulator of hepatic {MUFA} synthesis in
               obesity-linked diabetes.},
  author    = {Biddinger, Sudha B and Miyazaki, Makoto and Boucher, Jeremie and Ntambi,
               James M and Kahn, C Ronald},
  volume    = {55},
  number    = {7},
  pages     = {2032--41},
  year      = {2006},
  month     = {7},
  url       = {http://www.pubmed.org/16804073},
  pmid      = {16804073},
  doi       = {10.2337/db05-0742},
  keywords  = {Animals, Insulin, Mice, Body Weight, Leptin, Stearoyl-CoA Desaturase, Base
               Sequence, Blood Glucose, {DNA} Primers, Energy Intake, Mice, Knockout,
               Mice, Obese, Polymerase Chain Reaction, Receptor, Insulin, Receptors,
               Leptin, Sterol Regulatory Element Binding Protein 1},
  file      = {FULLTEXT:pdfs/000/000/000000014.pdf:PDF}
}

Paper  doi  abstract   bibtex   

@article{kitamura_comparative_2005,
	title = {Comparative study of the endocrine-disrupting activity of bisphenol {A} and 19 related compounds.},
	volume = {84},
	issn = {1096-6080},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/15635150},
	doi = {10.1093/toxsci/kfi074},
	abstract = {The endocrine-disrupting activities of bisphenol A (BPA) and 19 related compounds were comparatively examined by means of different in vitro and in vivo reporter assays. BPA and some related compounds exhibited estrogenic activity in human breast cancer cell line MCF-7, but there were remarkable differences in activity. Tetrachlorobisphenol A (TCBPA) showed the highest activity, followed by bisphenol B, BPA, and tetramethylbisphenol A (TMBPA); 2,2-bis(4-hydroxyphenyl)-1-propanol, 1,1-bis(4-hydroxyphenyl)propionic acid and 2,2-diphenylpropane showed little or no activity. Anti-estrogenic activity against 17beta-estradiol was observed with TMBPA and tetrabromobisphenol A (TBBPA). TCBPA, TBBPA, and BPA gave positive responses in the in vivo uterotrophic assay using ovariectomized mice. In contrast, BPA and some related compounds showed significant inhibitory effects on the androgenic activity of 5alpha-dihydrotestosterone in mouse fibroblast cell line NIH3T3. TMBPA showed the highest antagonistic activity, followed by bisphenol AF, bisphenol AD, bisphenol B, and BPA. However, TBBPA, TCBPA, and 2,2-diphenylpropane were inactive. TBBPA, TCBPA, TMBPA, and 3,3'-dimethylbisphenol A exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growth hormone in a thyroid hormone-dependent manner. However, BPA and other derivatives did not show such activity. The results suggest that the 4-hydroxyl group of the A-phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the 3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.},
	number = {2},
	journal = {Toxicological sciences},
	author = {Kitamura, Shigeyuki and Suzuki, Tomoharu and Sanoh, Seigo and Kohta, Ryuki and Jinno, Norimasa and Sugihara, Kazumi and Yoshihara, Shin'ichi and Fujimoto, Nariaki and Watanabe, Hiromitsu and Ohta, Shigeru},
	month = apr,
	year = {2005},
	pmid = {15635150},
	keywords = {Air Pollutants, Animals, Breast Neoplasms, Breast Neoplasms: drug therapy, Breast Neoplasms: metabolism, Dose-Response Relationship, Drug, Estrogens, Female, Flame retardants, Growth Hormone, Growth Hormone: metabolism, Hormone Antagonists, Hormone Antagonists: chemistry, Hormone Antagonists: classification, Hormone Antagonists: toxicity, Humans, Mice, NIH 3T3 Cells, NIH 3T3 Cells: drug effects, NIH 3T3 Cells: metabolism, Non-Steroidal, Non-Steroidal: chemistry, Non-Steroidal: classification, Non-Steroidal: toxicity, Occupational, Occupational: toxicity, Phenols, Phenols: chemistry, Phenols: classification, Phenols: toxicity, Pituitary Gland, Pituitary Gland: drug effects, Pituitary Gland: metabolism, Structure-Activity Relationship, Tumor, cell line, frelec, tox},
	pages = {249--59},
}

@Article{Backwell2004,
  author   = {Patricia R Y Backwell and Michael D Jennions},
  journal  = {Nature},
  title    = {Animal behaviour: {C}oalition among male fiddler crabs.},
  year     = {2004},
  number   = {6998},
  pages    = {417},
  volume   = {430},
  abstract = {Until now, no compelling evidence has emerged from studies of animal
	territoriality to indicate that a resident will strategically help
	a neighbour to defend its territory against an intruder. We show
	here that territory-owning Australian fiddler crabs will judiciously
	assist other crabs in defending their neighbouring territories. This
	cooperation supports the prediction that it is sometimes less costly
	to assist a familiar neighbour than to renegotiate boundaries with
	a new, and possibly stronger, neighbour.},
  doi      = {10.1038/430417a},
  keywords = {Animals, Attention, Brain, Decision Making, Face, Female, Haplorhini, Housing, Humans, Magnetic Resonance Imaging, Male, Models, Neurological, Pattern Recognition, Visual, Photic Stimulation, Prefrontal Cortex, Research Support, Non-U.S. Gov't, U.S. Gov't, P.H.S., Visual Perception, Choice Behavior, Cognition, Dopamine, Learning, Schizophrenia, Substance-Related Disorders, Generalization (Psychology), Motor Skills, Non-P.H.S., Nerve Net, Neuronal Plasticity, Perception, Cerebral Cortex, Memory, Neurons, Sound Localization, Synapses, Synaptic Transmission, Neural Pathways, Non-, Acoustic Stimulation, Adult, Age of Onset, Aging, Blindness, Child, Preschool, Infant, Newborn, Pitch Perception, Analysis of Variance, Animal Welfare, Laboratory, Behavior, Animal, Hybridization, Genetic, Maze Learning, Mice, Inbred C57BL, Inbred DBA, Phenotype, Reproducibility of Results, Darkness, Deafness, Finches, Sleep, Sound, Sunlight, Time Factors, Vocalization, Energy Metabolism, Evolution, Fossils, History, Ancient, Hominidae, Biological, Physical Endurance, Running, Skeleton, Walking, Acoustics, Auditory Perception, Cues, Discrimination Learning, Pair Bond, Social Behavior, Songbirds, Adolescent, England, Habituation (Psychophysiology), Korea, Language, Semantics, Vocabulary, Action Potentials, Hippocampus, Pyramidal Cells, Rats, Rotation, Australia, Brachyura, Cooperative Behavior, Logistic Models, Territoriality, 15269757},
}

Paper  doi  abstract   bibtex   

@article{Jacquemard2004,
	title = {Synthesis of diphenylcarbazoles as cytotoxic {DNA} binding agents.},
	volume = {2},
	issn = {1477-0520},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/15136803},
	doi = {10.1039/b401445f},
	abstract = {We report the synthesis of a series of novel diphenylcarbazoles designed to interact with DNA. The compounds bearing two or three dimethylaminoalkyloxy side chains were found to bind much more tightly to DNA, preferentially at AT-rich sites, than the corresponding hydroxy compounds. The DNA binding compounds exhibit potent cytotoxic activity toward P388 leukemia cells. The 3,6-diphenylcarbazole thus represent an interesting scaffold to develop antitumor agents interacting with nucleic acids.},
	number = {10},
	journal = {Organic \& biomolecular chemistry},
	author = {Jacquemard, Ulrich and Routier, Sylvain and Tatibouët, Arnaud and Kluza, Jérôme and Laine, William and Bal, Christine and Bailly, Christian and Mérour, Jean-Yves},
	month = may,
	year = {2004},
	pmid = {15136803},
	keywords = {\#nosource, Alkylation, Animals, Antineoplastic Agents, Antineoplastic Agents: chemical synthesis, Antineoplastic Agents: chemistry, Antineoplastic Agents: pharmacology, Apoptosis, Apoptosis: drug effects, Benzene Derivatives, Benzene Derivatives: chemical synthesis, Benzene Derivatives: chemistry, Benzene Derivatives: pharmacology, Carbazoles, Carbazoles: chemical synthesis, Carbazoles: chemistry, Cell Cycle, Cell Cycle: drug effects, Cell Division, Cell Division: drug effects, Cell Line, DNA, DNA: chemistry, Flow Cytometry, Heterocyclic Compounds with 4 or More Rings, Heterocyclic Compounds with 4 or More Rings: chemi, Heterocyclic Compounds with 4 or More Rings: pharm, Inhibitory Concentration 50, Magnetic Resonance Spectroscopy, Mice, Molecular Structure, Poly dA-dT, Poly dA-dT: chemistry, Structure-Activity Relationship, Transition Temperature, Transition Temperature: drug effects, Tumor},
	pages = {1476--83},
}

@article{den_brok_situ_2004,
	title = {In situ tumor ablation creates an antigen source for the generation of antitumor immunity},
	volume = {64},
	issn = {0008-5472},
	doi = {10.1158/0008-5472.CAN-03-3949},
	abstract = {Tumor-destructing techniques, like radiofrequency ablation (RFA), allow eradication of large tumors. Potentially, in situ tumor destruction also can provide the immune system with an antigen source for the induction of antitumor immunity. Antigen-presenting cells could take up antigens in the periphery after which they induce specific immune responses. Recent data show that especially antigen-presenting dendritic cells are crucial for the induction of potent immune responses. However, virtually nothing is known regarding the induction of immune responses after in situ tumor destruction in mice or humans. We used the well-defined murine B16-OVA melanoma cell line to develop a novel tumor model to explore: (a). the immunologic consequences of in situ tumor destruction; and (b). the efficacy of a combination approach of tumor destruction and immunostimulation. Applying this model system we demonstrate that following RFA, a weak but detectable immune response develops, directed against OVA, but also against a broader range of B16 antigens. Adoptive transfer experiments further indicate that antitumor reactivity can be transferred to naïve mice by splenocytes. To augment the response observed, we administered a blocking monoclonal antibody against cytotoxic T-lymphocyte-associated antigen 4 at the time of tumor destruction. Interestingly, this strongly enhanced antitumor immunity, resulting in long-lasting tumor protection. These results illustrate that in situ tumor destruction can provide a useful antigen source for the induction of antitumor immunity, provided that additional immunostimulatory signals are coadministered.},
	language = {eng},
	number = {11},
	journal = {Cancer Research},
	author = {den Brok, Martijn H. M. G. M. and Sutmuller, Roger P. M. and van der Voort, Robbert and Bennink, Erik J. and Figdor, Carl G. and Ruers, Theo J. M. and Adema, Gosse J.},
	month = jun,
	year = {2004},
	pmid = {15173017},
	keywords = {Animals, Antibodies, Monoclonal, Antigens, CD, Antigens, Differentiation, Antigens, Neoplasm, CTLA-4 Antigen, Catheter Ablation, Cricetinae, Female, Immunotherapy, Adoptive, Interferon-gamma, Lymphocyte Activation, Male, Melanoma, Experimental, Mice, Mice, Inbred C57BL, T-Lymphocytes},
	pages = {4024--4029},
}

@Article{Mellars2004,
  author   = {Paul Mellars},
  journal  = {Nature},
  title    = {Neanderthals and the modern human colonization of {E}urope.},
  year     = {2004},
  number   = {7016},
  pages    = {461-5},
  volume   = {432},
  abstract = {The fate of the Neanderthal populations of Europe and western Asia
	has gripped the popular and scientific imaginations for the past
	century. Following at least 200,000 years of successful adaptation
	to the glacial climates of northwestern Eurasia, they disappeared
	abruptly between 30,000 and 40,000 years ago, to be replaced by populations
	all but identical to modern humans. Recent research suggests that
	the roots of this dramatic population replacement can be traced far
	back to events on another continent, with the appearance of distinctively
	modern human remains and artefacts in eastern and southern Africa.},
  doi      = {10.1038/nature03103},
  keywords = {Animals, Attention, Brain, Decision Making, Face, Female, Haplorhini, Housing, Humans, Magnetic Resonance Imaging, Male, Models, Neurological, Pattern Recognition, Visual, Photic Stimulation, Prefrontal Cortex, Research Support, Non-U.S. Gov't, U.S. Gov't, P.H.S., Visual Perception, Choice Behavior, Cognition, Dopamine, Learning, Schizophrenia, Substance-Related Disorders, Generalization (Psychology), Motor Skills, Non-P.H.S., Nerve Net, Neuronal Plasticity, Perception, Cerebral Cortex, Memory, Neurons, Sound Localization, Synapses, Synaptic Transmission, Neural Pathways, Non-, Acoustic Stimulation, Adult, Age of Onset, Aging, Blindness, Child, Preschool, Infant, Newborn, Pitch Perception, Analysis of Variance, Animal Welfare, Laboratory, Behavior, Animal, Hybridization, Genetic, Maze Learning, Mice, Inbred C57BL, Inbred DBA, Phenotype, Reproducibility of Results, Darkness, Deafness, Finches, Sleep, Sound, Sunlight, Time Factors, Vocalization, Energy Metabolism, Evolution, Fossils, History, Ancient, Hominidae, Biological, Physical Endurance, Running, Skeleton, Walking, Acoustics, Auditory Perception, Cues, Discrimination Learning, Pair Bond, Social Behavior, Songbirds, Adolescent, England, Habituation (Psychophysiology), Korea, Language, Semantics, Vocabulary, Action Potentials, Hippocampus, Pyramidal Cells, Rats, Rotation, Australia, Brachyura, Cooperative Behavior, Logistic Models, Territoriality, Africa, Archaeology, Emigration and Immigration, Europe, Geography, Phylogeny, Population Dynamics, 15565144},
}

@article{ santarelli_requirement_2003,
  title = {Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants},
  volume = {301},
  issn = {1095-9203},
  doi = {10.1126/science.1083328},
  abstract = {Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.},
  language = {eng},
  number = {5634},
  journal = {Science (New York, N.Y.)},
  author = {Santarelli, Luca and Saxe, Michael and Gross, Cornelius and Surget, Alexandre and Battaglia, Fortunato and Dulawa, Stephanie and Weisstaub, Noelia and Lee, James and Duman, Ronald and Arancio, Ottavio and Belzung, Catherine and Hen, René},
  month = {August},
  year = {2003},
  pmid = {12907793},
  keywords = {8-Hydroxy-2-(di-n-propylamino)tetralin, Animals, Antidepressive Agents, Antidepressive Agents, Second-Generation, Antidepressive Agents, Tricyclic, Behavior, Animal, Cell Division, Conditioning (Psychology), Dentate Gyrus, Fear, Feeding Behavior, Fluoxetine, Grooming, Hippocampus, Long-Term Potentiation, Male, Mice, Mice, Knockout, Neurons, Receptors, Serotonin, Receptors, Serotonin, 5-{HT}1, Stress, Physiological, Synaptic Transmission},
  pages = {805--809}
}

@article{witczak_thio-sugars_2003,
	title = {Thio-sugars {VII}. {Effect} of 3-deoxy-4-{S}-(beta-{D}-gluco- and beta-{D}-galactopyranosyl)-4-thiodisaccharides and their sulfoxides and sulfones on the viability and growth of selected murine and human tumor cell lines},
	volume = {338},
	issn = {0008-6215},
	abstract = {The first conversion of (1--{\textgreater}4)-thiodisaccharides into corresponding sulfoxides and sulfones by conventional oxidation with m-chloroperoxybenzoic acid (MCPBA) is reported. The effects of alpha-(1--{\textgreater}4)-3'-deoxythiodisaccharides (8-9) and their sulfoxide (14-15) and sulfone (16-17) derivatives on murine leukemia and human colon and pancreatic carcinoma cell viability were studied. Concentrations of thio-sugars that decreased tumor cell line viability by 50\% (IC(50)), measured via the MTT assay, ranged from 6.4 to 38.3 microg/mL. The effect of alpha-(1--{\textgreater}4)-3'-deoxythiodisaccharide derivatives were most profound on human pancreatic epithelial carcinoma (PANC-1) cells with compounds 8 and 9 having IC(50) values of 6.4 microg/mL and 8.2 microg/mL, respectively. Sulfone derivatives 16 and 17 also had pronounced effects on PANC-1 cell viability (IC(50)=10.2 microg/mL and 9.6 microg/mL, respectively). These results indicate that deoxythio-disaccharide analogs generated by functionalization of the universal chiral precursor levoglucosenone may have cytotoxic properties and therapeutic potential as anticancer agents.},
	language = {eng},
	number = {1},
	journal = {Carbohydrate Research},
	author = {Witczak, Zbigniew J. and Kaplon, Peter and Dey, P. Markus},
	month = jan,
	year = {2003},
	pmid = {12504376},
	keywords = {Animals, Antineoplastic Agents, Carbohydrates, Cell Division, Cell Survival, Humans, Inhibitory Concentration 50, Mice, Structure-Activity Relationship, Sulfhydryl Compounds, Sulfones, Sulfoxides, Tumor Cells, Cultured},
	pages = {11--18},
}

Paper  abstract   bibtex   

@article{Meyer2003,
	title = {Brain imaging: {How} stable are synaptic connections?},
	volume = {13},
	issn = {0960-9822},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/12620207},
	abstract = {Cortical circuits can undergo experience-dependent remodeling, while retaining the capacity for long-term information storage. The stability of individual synaptic connections is fundamental to both processes, but poorly understood; two studies using new in vivo imaging techniques have finally shed some light on this important issue.},
	number = {5},
	urldate = {2014-05-30},
	journal = {Current biology},
	author = {Meyer, MP and Niell, CM and Smith, SJ},
	month = mar,
	year = {2003},
	pmid = {12620207},
	keywords = {Animals, Brain, Brain: anatomy \& histology, Dendrites, Diagnostic Imaging, Mice, Synapses},
	pages = {R180--2},
}

@article{ ducottet_effects_2003,
  title = {Effects of the selective nonpeptide corticotropin-releasing factor receptor 1 antagonist antalarmin in the chronic mild stress model of depression in mice},
  volume = {27},
  issn = {0278-5846},
  doi = {10.1016/S0278-5846(03)00051-4},
  abstract = {Several recent studies on corticotropin-releasing factor ({CRF}) have suggested that this neuropeptide may play a role in depression. Consequently, {CRF} receptor antagonists have been proposed as potential new agents for the treatment of this condition. This study investigated the effects of a 4-week treatment with the well-known {CRF}(1) receptor antagonist, antalarmin, and the prototypical selective serotonin reuptake inhibitor ({SSRI}), fluoxetine, in the chronic mild stress ({CMS}) model in {BALB}/c mice. Animals were exposed to 9 weeks of {CMS} which rapidly (within 2 weeks) produced decrease of physical state ({PS}), body weight gain and blunted emotional response in the light/dark test. Chronic treatment with antalarmin (10 mg/kg ip) and fluoxetine (10 mg/kg ip) led to an improvement of {CMS}-induced modifications. These results suggest that {CRF}(1) receptor antagonists may represent potential antidepressants.},
  language = {eng},
  number = {4},
  journal = {Progress in Neuro-Psychopharmacology \& Biological Psychiatry},
  author = {Ducottet, Cecile and Griebel, Guy and Belzung, Catherine},
  month = {June},
  year = {2003},
  pmid = {12787849},
  keywords = {Animals, Depression, Disease Models, Animal, Drug Therapy, Combination, Fluoxetine, Male, Mice, Mice, Inbred {BALB} C, Pyrimidines, Pyrroles, Receptors, Corticotropin-Releasing Hormone, Serotonin Uptake Inhibitors, Stress, Psychological},
  pages = {625--631}
}

@Article{Ivan_2002_1345,
  author = {Ivan, Eugen and Khatri, Jaikirshan J. and Johnson, Chad and Magid, Richard and Godin, Denis and Nandi, Sudeshna and Lessner, Susan and Galis, Zorina S.},
 journal = {Circulation},
 note = {10.1161/01.CIR.0000016825.17448.11 NOT IN FILE},
 number = {22},
 pages = {2686-2691},
 title = {Expansive arterial remodeling is associated with increased neointimal macrophage foam cell content: {T}he murine model of macrophage-rich carotid artery lesions},
 volume = {105},
 year = {2002},
 keywords = {Arteries, Carotid, Arteries, Macrophages, Matrix, Metalloproteinases, methods, Mice},
 title_with_no_special_chars = {Expansive Arterial Remodeling Is Associated With Increased Neointimal Macrophage Foam Cell Content The Murine Model of MacrophageRich Carotid Artery Lesions}
}

@article{ clement_genetic_2002,
  title = {Genetic basis of anxiety-like behaviour: a critical review},
  volume = {57},
  issn = {0361-9230},
  shorttitle = {Genetic basis of anxiety-like behaviour},
  abstract = {The way genetic and/or environmental factors influence psychiatric disorders is an enduring question in the field of human psychiatric diseases. Anxiety-related disorders provide a relevant example of how such an interaction is involved in the aetiology of a psychiatric disease. In this paper we review the literature on that subject, reporting data derived from human and rodent studies. We present in a critical way the animal models used in the studies aimed at investigating the genetic basis of anxiety, including inbred mice, selected lines, multiple marker strains, or knockout mice and review data reporting environmental components influencing anxiety-related behaviours. We conclude that anxiety is a complex behaviour, underlined not only by genetic or environmental factors but also by multiple interactions between these two factors.},
  language = {eng},
  number = {1},
  journal = {Brain Research Bulletin},
  author = {Clément, Yan and Calatayud, François and Belzung, Catherine},
  month = {January},
  year = {2002},
  pmid = {11827738},
  keywords = {Animals, Anxiety, Chromosome Mapping, Disease Models, Animal, Environment, Gene Targeting, Genetic Predisposition to Disease, Humans, Mice, Mice, Inbred Strains, Neurotransmitter Agents, Rats},
  pages = {57--71}
}

Paper  doi  abstract   bibtex   

@article{steiniger_perifollicular_2001,
	title = {The perifollicular and marginal zones of the human splenic white pulp : do fibroblasts guide lymphocyte immigration?},
	volume = {159},
	issn = {0002-9440},
	shorttitle = {The perifollicular and marginal zones of the human splenic white pulp},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/11485909},
	doi = {10.1016/S0002-9440(10)61722-1},
	abstract = {We investigate the white pulp compartments of 73 human spleens and demonstrate that there are several microanatomical peculiarities in man that do not occur in rats or mice. Humans lack a marginal sinus separating the marginal zone (MZ) from the follicles or the follicular mantle zone. The MZ is divided into an inner and an outer compartment by a special type of fibroblasts. An additional compartment, termed the perifollicular zone, is present between the follicular MZ and the red pulp. The perifollicular zone contains sheathed capillaries and blood-filled spaces without endothelial lining. In the perifollicular zone, in the outer MZ, and in the T cell zone fibroblasts of an unusual phenotype occur. These cells stain for the adhesion molecules MAdCAM-1, VCAM-1 (CD106), and VAP-1; the Thy-1 (CD90) molecule; smooth muscle alpha-actin and smooth muscle myosin; cytokeratin 18; and thrombomodulin (CD141). They are, however, negative for the peripheral node addressin, the cutaneous lymphocyte antigen, CD34, PECAM-1 (CD31), and P- and E-selectin (CD62P and CD62E). In the MZ the fibroblasts are often tightly associated with CD4-positive T lymphocytes, whereas CD8-positive cells are almost absent. Our findings lead to the hypothesis, that recirculating CD4-positive T lymphocytes enter the human splenic white pulp from the open circulation of the perifollicular zone without crossing an endothelium. Specialized fibroblasts may attract these T cells and guide them into the periarteriolar T cell area.},
	number = {2},
	urldate = {2012-03-26},
	journal = {The American Journal of Pathology},
	author = {Steiniger, B and Barth, P and Hellinger, A},
	month = aug,
	year = {2001},
	pmid = {11485909},
	keywords = {Actins, Adult, Animals, Antigens, CD, Biological Markers, Cell Adhesion Molecules, Female, Fibroblasts, Humans, Keratins, Lymphocytes, Male, Mice, Myosins, Rats, Spleen, Splenectomy},
	pages = {501--512},
}

Paper  Website  abstract   bibtex   

@article{
 title = {Understanding human disease mutations through the use of interspecific genetic variation},
 type = {article},
 year = {2001},
 identifiers = {[object Object]},
 keywords = {*Evolution, Molecular,Amino Acids/genetics,Animals,Cattle,Cricetinae,Cystic Fibrosis Transmembrane Conductance Regulato,Databases, Nucleic Acid,Eye Proteins/genetics,Gene Frequency,Genetic Predisposition to Disease/*genetics,Glucosephosphate Dehydrogenase/genetics,Homeodomain Proteins/genetics,Humans,Leukocyte L1 Antigen Complex,Membrane Glycoproteins/genetics,Mice,Mutation,Neural Cell Adhesion Molecules/genetics,Paired Box Transcription Factors,Phenylalanine Hydroxylase/genetics,Phylogeny,Polymorphism, Single Nucleotide,Rats,Repressor Proteins/genetics,Research Support, Non-U.S. Gov't,Research Support, U.S. Gov't, Non-P.H.S.,Research Support, U.S. Gov't, P.H.S.,Species Specificity,Tumor Suppressor Proteins,Variation (Genetics)},
 pages = {2319-2328},
 volume = {10},
 websites = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11689479},
 id = {615db8bf-ae06-347d-a726-890771c0ab9a},
 created = {2017-06-19T13:46:04.109Z},
 file_attached = {true},
 profile_id = {de68dde1-2ff3-3a4e-a214-ef424d0c7646},
 group_id = {b2078731-0913-33b9-8902-a53629a24e83},
 last_modified = {2017-06-19T13:46:04.233Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 source_type = {Journal Article},
 notes = {<m:note>0964-6906 (Print)<m:linebreak/>Journal Article</m:note>},
 abstract = {Data on replacement mutations in genes of disease patients exist in a variety of online resources. In addition, genome sequencing projects and individual gene sequencing efforts have led to the identification of disease gene homologs in diverse metazoan species. The availability of these two types of information provides unique opportunities to investigate factors that are important in the development of genetically based disease by contrasting long and short-term molecular evolutionary patterns. Therefore, we conducted an analysis of disease-associated human genetic variation for seven disease genes: the cystic fibrosis transmembrane conductance regulator, glucose-6-phosphate dehydrogenase, the neural cell adhesion molecule L1, phenylalanine hydroxylase, paired box 6, the X-linked retinoschisis gene and TSC2/tuberin. Our analyses indicate that disease mutations show definite patterns when examined from an evolutionary perspective. Human replacement mutations resulting in disease are overabundant at amino acid positions most conserved throughout the long-term history of metazoans. In contrast, human polymorphic replacement mutations and silent mutations are randomly distributed across sites with respect to the level of conservation of amino acid sites within genes. Furthermore, disease-causing amino acid changes are of types usually not observed among species. Using Grantham's chemical difference matrix, we find that amino acid changes observed in disease patients are far more radical than the variation found among species and in non-diseased humans. Overall, our results demonstrate the usefulness of evolutionary analyses for understanding patterns of human disease mutations and underscore the biomedical significance of sequence data currently being generated from various model organism genome sequencing projects.},
 bibtype = {article},
 author = {Miller, M P and Kumar, S},
 journal = {Hum Mol Genet},
 number = {21}
}

Paper  Website  abstract   bibtex   

@article{
 title = {Conditional inactivation of Fgf4 reveals complexity of signalling during limb bud development.},
 type = {article},
 year = {2000},
 identifiers = {[object Object]},
 keywords = {Animals,DNA-Binding Proteins,DNA-Binding Proteins: genetics,Ectoderm,Ectoderm: metabolism,Ectoderm: physiology,Egg Proteins,Egg Proteins: genetics,Feedback,Feedback: physiology,Fibroblast Growth Factor 4,Fibroblast Growth Factors,Fibroblast Growth Factors: genetics,Fibroblast Growth Factors: metabolism,Gene Expression Regulation, Developmental,Genes, Lethal,Hedgehog Proteins,Homeodomain Proteins,Integrases,Integrases: genetics,Limb Buds,Limb Buds: embryology,Membrane Glycoproteins,Membrane Glycoproteins: genetics,Mice,Mice, Inbred C57BL,Mice, Knockout,Mice, Transgenic,Proteins,Proteins: genetics,Proto-Oncogene Proteins,Proto-Oncogene Proteins: genetics,Proto-Oncogene Proteins: metabolism,Receptors, Cell Surface,Signal Transduction,Signal Transduction: genetics,Trans-Activators,Viral Proteins,Zona Pellucida,Zona Pellucida: physiology},
 pages = {83-6},
 volume = {25},
 websites = {http://www.ncbi.nlm.nih.gov/pubmed/10802662},
 month = {5},
 id = {80cc23bf-01ef-371f-aca0-1552efb115d3},
 created = {2016-04-08T12:19:42.000Z},
 file_attached = {true},
 profile_id = {994bc413-6766-31df-917a-32165aa30f6c},
 group_id = {cec5aa9e-65e1-3c21-bc44-78fa6504020e},
 last_modified = {2017-03-14T10:42:46.538Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Sun2000},
 folder_uuids = {37786225-e8d4-483b-be04-dfc97f200748},
 private_publication = {false},
 abstract = {Development of the vertebrate limb bud depends on reciprocal interactions between the zone of polarizing activity (ZPA) and the apical ectodermal ridge (AER). Sonic hedgehog (SHH) and fibroblast growth factors (FGFs) are key signalling molecules produced in the ZPA and AER, respectively. Experiments in chicks suggested that SHH expression in the ZPA is maintained by FGF4 expression in the AER, and vice versa, providing a molecular mechanism for coordinating the activities of these two signalling centres. This SHH/FGF4 feedback loop model is supported by genetic evidence showing that Fgf4 expression is not maintained in Shh-/- mouse limbs. We report here that Shh expression is maintained and limb formation is normal when Fgf4 is inactivated in mouse limbs, thus contradicting the model. We also found that maintenance of Fgf9 and Fgf17 expression is dependent on Shh, whereas Fgf8 expression is not. We discuss a model in which no individual Fgf expressed in the AER (AER-Fgf) is solely necessary to maintain Shh expression, but, instead, the combined activities of two or more AER-Fgfs function in a positive feedback loop with Shh to control limb development.},
 bibtype = {article},
 author = {Sun, X and Lewandoski, M and Meyers, E N and Liu, Y H and Maxson, R E and Martin, G R},
 journal = {Nature genetics},
 number = {1}
}

@article{rogakou_dna_1998,
	title = {{DNA} double-stranded breaks induce histone {H2AX} phosphorylation on serine 139},
	volume = {273},
	issn = {0021-9258},
	abstract = {When mammalian cell cultures or mice are exposed to ionizing radiation in survivable or lethal amounts, novel mass components are found in the histone H2A region of two-dimensional gels. Collectively referred to as gamma, these components are formed in vivo by several procedures that introduce double-stranded breaks into DNA. gamma-Components, which appeared to be the only major novel components detected by mass or 32PO4 incorporation on acetic acid-urea-Triton X-100-acetic acid-urea-cetyltrimethylammonium bromide or SDS-acetic acid-urea-cetyltrimethylammonium bromide gels after exposure of cells to ionizing radiation, are shown to be histone H2AX species that have been phosphorylated specifically at serine 139. gamma-H2AX appears rapidly after exposure of cell cultures to ionizing radiation; half-maximal amounts are reached by 1 min and maximal amounts by 10 min. At the maximum, approximately 1\% of the H2AX becomes gamma-phosphorylated per gray of ionizing radiation, a finding that indicates that 35 DNA double-stranded breaks, the number introduced by each gray into the 6 x 10(9) base pairs of a mammalian G1 genome, leads to the gamma-phosphorylation of H2AX distributed over 1\% of the chromatin. Thus, about 0.03\% of the chromatin appears to be involved per DNA double-stranded break. This value, which corresponds to about 2 x 10(6) base pairs of DNA per double-stranded break, indicates that large amounts of chromatin are involved with each DNA double-stranded break. Thus, gamma-H2AX formation is a rapid and sensitive cellular response to the presence of DNA double-stranded breaks, a response that may provide insight into higher order chromatin structures.},
	language = {eng},
	number = {10},
	journal = {The Journal of Biological Chemistry},
	author = {Rogakou, E. P. and Pilch, D. R. and Orr, A. H. and Ivanova, V. S. and Bonner, W. M.},
	month = mar,
	year = {1998},
	keywords = {Amino Acid Sequence, Animals, Cells, Cultured, Chromatin, DNA, Electrophoresis, Gel, Two-Dimensional, Gamma Rays, Histones, Mice, Mice, Inbred Strains, Molecular Sequence Data, Nuclear Proteins, Peptide Fragments, Phosphorylation, Phosphoserine, Protein Kinases, Recombinant Proteins, Whole-Body Irradiation},
	pages = {5858--5868},
}

@Article{Nakashima_1994_1801,
  author = {Nakashima, Y. and Plump, A. S. and Raines, E. W. and Breslow, J. L. and Ross, R.},
 journal = {Arterioscler.Thromb.},
 note = {DA - 19940204 NOT IN FILE},
 number = {1},
 pages = {133-140},
 title = {Apoe-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree},
 volume = {14},
 year = {1994},
 keywords = {Animals, Aorta, Aorta, Thoracic, Apolipoproteins, E, Arteries, Arteriosclerosis, Atherosclerosis, Carotid, Arteries, Connective, Tissue, Coronary, Vessels, deficiency, Diet, Endothelium, Vascular, etiology, Humans, Hypercholesterolemia, Leukocytes, Mononuclear, Macrophages, Mice, Mice, Inbred, BALB, C, Mice, Inbred, C57BL, Mice, Transgenic, Microscopy, Electron, pathology, Pulmonary, Artery, Research, Support, Non-U.S.Gov't, Research, Support, U.S.Gov't, P.H.S., therapy},
 title_with_no_special_chars = {ApoEdeficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree}
}

@Article{Zhang_1994_1781,
  author = {Zhang, S. H. and Reddick, R. L. and Burkey, B. and Maeda, N.},
 journal = {J.Clin.Invest},
 note = {DA - 19941013 NOT IN FILE},
 number = {3},
 pages = {937-945},
 title = {Diet-induced atherosclerosis in mice heterozygous and homozygous for apolipoprotein E gene disruption},
 volume = {94},
 year = {1994},
 keywords = {Animals, Aorta, Apolipoproteins, E, Arteries, Arteriosclerosis, Atherosclerosis, blood, Cholesterol, Comparative, Study, Diet, Diet, Atherogenic, Female, genetics, Heterozygote, Homozygote, Humans, Lipoproteins, Lipoproteins, HDL, Cholesterol, Liver, Macrophages, Male, metabolism, Mice, Mice, Inbred, C57BL, Mice, Inbred, Strains, Mice, Mutant, Strains, Muscle, Smooth, Vascular, pathology, Reference, Values, Research, Support, Non-U.S.Gov't, Research, Support, U.S.Gov't, P.H.S., Triglycerides, ultrastructure},
 title_with_no_special_chars = {Dietinduced atherosclerosis in mice heterozygous and homozygous for apolipoprotein E gene disruption}
}

Website  bibtex   

@article{
 title = {DNA binding study of isophorone in rats and mice},
 type = {article},
 year = {1990},
 identifiers = {[object Object]},
 keywords = {Animals,Cyclohexanones/*metabolism,DNA/*metabolism,Female,Male,Mice,Rats,Rats, Inbred F344},
 pages = {684-685},
 volume = {64},
 websites = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2090039},
 edition = {1990/01/01},
 id = {be1a97a7-cc9c-3bef-a0c9-625b8898ee26},
 created = {2017-06-19T13:43:15.318Z},
 file_attached = {false},
 profile_id = {de68dde1-2ff3-3a4e-a214-ef424d0c7646},
 group_id = {b2078731-0913-33b9-8902-a53629a24e83},
 last_modified = {2017-06-19T13:43:15.427Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 source_type = {Journal Article},
 language = {eng},
 notes = {<m:note>Thier, R<m:linebreak/>Peter, H<m:linebreak/>Wiegand, H J<m:linebreak/>Bolt, H M<m:linebreak/>Letter<m:linebreak/>Germany<m:linebreak/>Archives of toxicology<m:linebreak/>Arch Toxicol. 1990;64(8):684-5.</m:note>},
 bibtype = {article},
 author = {Thier, R and Peter, H and Wiegand, H J and Bolt, H M},
 journal = {Arch Toxicol},
 number = {8}
}

Paper  abstract   bibtex   

@article{schallreuter_azelaic_1987,
	title = {Azelaic acid as a competitive inhibitor of thioredoxin reductase in human melanoma cells},
	volume = {36},
	issn = {0304-3835},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/3652030},
	abstract = {Azelaic acid has been shown to inhibit thioredoxin reductase (TR) at the surface of guinea pig and human skin, on cultures of human keratinocytes, melanocytes, melanoma cells, murine melanoma cells (Cloudman S91), and on purified enzymes from Escherichia coli, rat liver, and human melanoma. Human melanoma cells are more resistant to inhibition by azelaic acid than murine melanoma or human melanocytes. Kinetic studies with pure TRs indicate that azelaic acid is a reversible competitive inhibitor. Fluorescence spectroscopy has been used to show that azelaic acid does not interfere with electron transfer from NADPH to FAD on TR. However, azelaic acid does inhibit electron transfer from the dithiolate active site of this enzyme. Inhibition by azelaic acid is pH-dependent, requiring the dissociation of both carboxylate groups, and also the dissociation of the active site dithiol groups. Binding studies with [14C]azelaic acid at different pHs, indicate that inhibition is first due to the formation of a thioester on the active thiolate groups followed by transacylation of a basic amino acid residue in the active site. A comparative study of TR inhibition by C6, C9, C10 and C12 saturated dicarboxylic acids was also determined on guinea pig skin in vivo. These homologous dicarboxylic acids gave greater inhibition with increasing size (i.e. mol wt.).},
	number = {3},
	urldate = {2012-07-19},
	journal = {Cancer letters},
	author = {Schallreuter, K U and Wood, J M},
	month = sep,
	year = {1987},
	pmid = {3652030},
	keywords = {Animals, Cells, Cultured, Dicarboxylic Acids, Electron Transport, Guinea Pigs, Humans, Melanocytes, Melanoma, Mice, NADH, NADPH Oxidoreductases, Skin, Spectrometry, Fluorescence, Thioredoxin-Disulfide Reductase},
	pages = {297--305},
}

@article{mosmann_rapid_1983,
	title = {Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays},
	volume = {65},
	issn = {0022-1759},
	shorttitle = {Rapid colorimetric assay for cellular growth and survival},
	abstract = {A tetrazolium salt has been used to develop a quantitative colorimetric assay for mammalian cell survival and proliferation. The assay detects living, but not dead cells and the signal generated is dependent on the degree of activation of the cells. This method can therefore be used to measure cytotoxicity, proliferation or activation. The results can be read on a multiwell scanning spectrophotometer (ELISA reader) and show a high degree of precision. No washing steps are used in the assay. The main advantages of the colorimetric assay are its rapidity and precision, and the lack of any radioisotope. We have used the assay to measure proliferative lymphokines, mitogen stimulations and complement-mediated lysis.},
	language = {eng},
	number = {1-2},
	journal = {Journal of Immunological Methods},
	author = {Mosmann, T.},
	month = dec,
	year = {1983},
	pmid = {6606682},
	keywords = {Animals, Cell Line, Cell Survival, Colorimetry, Concanavalin A, Cytotoxicity Tests, Immunologic, Dose-Response Relationship, Immunologic, Interleukin-2, Lipopolysaccharides, Lymphocyte Activation, Lymphocytes, Lymphoma, Macrophage Activation, Mice, Mice, Inbred BALB C, Tetrazolium Salts, Thiazoles},
	pages = {55--63},
}