@article{Islam2014,
	title = {c-{Myc} quadruplex-forming sequence {Pu}-27 induces extensive damage in both telomeric and non-telomeric regions of {DNA}.},
	issn = {1083-351X},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/24464582},
	doi = {10.1074/jbc.m113.505073},
	abstract = {ABSTRACT Quadruplex-forming DNA sequences are present throughout the eukaryotic genome, including in telomeric DNA. We have shown c-myc promoter quadruplex-forming sequence, Pu-27, selectively kills transformed cells (Sedoris et al., 2012). In this study, we show that Pu-27 induces profound DNA damage resulting in striking chromosomal abnormalities in the form of chromatid or chromosomal breaks, radial formation, telomeric DNA loss which induces γ-H2AX in U937 cells. Pu-27 down regulates telomeric shelterin proteins, DNA damage response mediators (RAD17 and RAD50), double strand break (DSB) repair molecule 53BP1, G2 checkpoint regulators (CHK1 and CHK2) and anti-apoptosis gene survivin. Interestingly, there are no changes of DNA repair molecules H2AX, BRCA1 and the telomere maintenance gene, hTERT. delta-B-U937, where U937 cells stably transfected with deleted basic-domain of TRF2 is partially sensitive to Pu-27 but exhibits no changes in expression of shelterin proteins. However, there is an up-regulation of CHK1, CHK2, H2AX, BRCA1, and survivin. TIF (Telomere-dysfunction Induced Foci) assay revealed co-association of TRF1with gamma-H2AX in ATM deficient cells which are differentially sensitive to Pu-27 than ATM proficient cells. Alt (Alternating Lengthening of Telomere) cells are relatively resistant to Pu-27 but no significant changes of telomerase activity in both Alt and non-Alt cells. Lastly, we show this Pu-27 mediated sensitivity is P53 independent. The data therefore support two conclusions. Firstly, Pu-27 induces DNA damage within both telomeric and non-telomeric regions of the genome. Secondly, Pu-27 mediated telomeric damage is due, at least in part, to compromise of the telomeric shelterin protein complex.},
	journal = {The Journal of biological chemistry},
	author = {Islam, Md Ashraful and Thomas, Shelia D and Murty, Vundavalli V and Sedoris, Kara J and Miller, Donald M},
	month = jan,
	year = {2014},
	pmid = {24464582},
	keywords = {\#nosource, alt, cell death, complex, dna damage, g-quadruplex, myc, shelterin, survivin, telomeres},
}

{"_id":"emCWpK4bJWBspMhnJ","bibbaseid":"islam-thomas-murty-sedoris-miller-cmycquadruplexformingsequencepu27inducesextensivedamageinbothtelomericandnontelomericregionsofdna-2014","author_short":["Islam, M. A.","Thomas, S. D","Murty, V. V","Sedoris, K. J","Miller, D. M"],"bibdata":{"bibtype":"article","type":"article","title":"c-Myc quadruplex-forming sequence Pu-27 induces extensive damage in both telomeric and non-telomeric regions of DNA.","issn":"1083-351X","url":"http://www.ncbi.nlm.nih.gov/pubmed/24464582","doi":"10.1074/jbc.m113.505073","abstract":"ABSTRACT Quadruplex-forming DNA sequences are present throughout the eukaryotic genome, including in telomeric DNA. We have shown c-myc promoter quadruplex-forming sequence, Pu-27, selectively kills transformed cells (Sedoris et al., 2012). In this study, we show that Pu-27 induces profound DNA damage resulting in striking chromosomal abnormalities in the form of chromatid or chromosomal breaks, radial formation, telomeric DNA loss which induces γ-H2AX in U937 cells. Pu-27 down regulates telomeric shelterin proteins, DNA damage response mediators (RAD17 and RAD50), double strand break (DSB) repair molecule 53BP1, G2 checkpoint regulators (CHK1 and CHK2) and anti-apoptosis gene survivin. Interestingly, there are no changes of DNA repair molecules H2AX, BRCA1 and the telomere maintenance gene, hTERT. delta-B-U937, where U937 cells stably transfected with deleted basic-domain of TRF2 is partially sensitive to Pu-27 but exhibits no changes in expression of shelterin proteins. However, there is an up-regulation of CHK1, CHK2, H2AX, BRCA1, and survivin. TIF (Telomere-dysfunction Induced Foci) assay revealed co-association of TRF1with gamma-H2AX in ATM deficient cells which are differentially sensitive to Pu-27 than ATM proficient cells. Alt (Alternating Lengthening of Telomere) cells are relatively resistant to Pu-27 but no significant changes of telomerase activity in both Alt and non-Alt cells. Lastly, we show this Pu-27 mediated sensitivity is P53 independent. The data therefore support two conclusions. Firstly, Pu-27 induces DNA damage within both telomeric and non-telomeric regions of the genome. Secondly, Pu-27 mediated telomeric damage is due, at least in part, to compromise of the telomeric shelterin protein complex.","journal":"The Journal of biological chemistry","author":[{"propositions":[],"lastnames":["Islam"],"firstnames":["Md","Ashraful"],"suffixes":[]},{"propositions":[],"lastnames":["Thomas"],"firstnames":["Shelia","D"],"suffixes":[]},{"propositions":[],"lastnames":["Murty"],"firstnames":["Vundavalli","V"],"suffixes":[]},{"propositions":[],"lastnames":["Sedoris"],"firstnames":["Kara","J"],"suffixes":[]},{"propositions":[],"lastnames":["Miller"],"firstnames":["Donald","M"],"suffixes":[]}],"month":"January","year":"2014","pmid":"24464582","keywords":"#nosource, alt, cell death, complex, dna damage, g-quadruplex, myc, shelterin, survivin, telomeres","bibtex":"@article{Islam2014,\n\ttitle = {c-{Myc} quadruplex-forming sequence {Pu}-27 induces extensive damage in both telomeric and non-telomeric regions of {DNA}.},\n\tissn = {1083-351X},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/24464582},\n\tdoi = {10.1074/jbc.m113.505073},\n\tabstract = {ABSTRACT Quadruplex-forming DNA sequences are present throughout the eukaryotic genome, including in telomeric DNA. We have shown c-myc promoter quadruplex-forming sequence, Pu-27, selectively kills transformed cells (Sedoris et al., 2012). In this study, we show that Pu-27 induces profound DNA damage resulting in striking chromosomal abnormalities in the form of chromatid or chromosomal breaks, radial formation, telomeric DNA loss which induces γ-H2AX in U937 cells. Pu-27 down regulates telomeric shelterin proteins, DNA damage response mediators (RAD17 and RAD50), double strand break (DSB) repair molecule 53BP1, G2 checkpoint regulators (CHK1 and CHK2) and anti-apoptosis gene survivin. Interestingly, there are no changes of DNA repair molecules H2AX, BRCA1 and the telomere maintenance gene, hTERT. delta-B-U937, where U937 cells stably transfected with deleted basic-domain of TRF2 is partially sensitive to Pu-27 but exhibits no changes in expression of shelterin proteins. However, there is an up-regulation of CHK1, CHK2, H2AX, BRCA1, and survivin. TIF (Telomere-dysfunction Induced Foci) assay revealed co-association of TRF1with gamma-H2AX in ATM deficient cells which are differentially sensitive to Pu-27 than ATM proficient cells. Alt (Alternating Lengthening of Telomere) cells are relatively resistant to Pu-27 but no significant changes of telomerase activity in both Alt and non-Alt cells. Lastly, we show this Pu-27 mediated sensitivity is P53 independent. The data therefore support two conclusions. Firstly, Pu-27 induces DNA damage within both telomeric and non-telomeric regions of the genome. Secondly, Pu-27 mediated telomeric damage is due, at least in part, to compromise of the telomeric shelterin protein complex.},\n\tjournal = {The Journal of biological chemistry},\n\tauthor = {Islam, Md Ashraful and Thomas, Shelia D and Murty, Vundavalli V and Sedoris, Kara J and Miller, Donald M},\n\tmonth = jan,\n\tyear = {2014},\n\tpmid = {24464582},\n\tkeywords = {\\#nosource, alt, cell death, complex, dna damage, g-quadruplex, myc, shelterin, survivin, telomeres},\n}\n\n","author_short":["Islam, M. A.","Thomas, S. D","Murty, V. V","Sedoris, K. J","Miller, D. 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