@ARTICLE{Pursglove20052472,
author={Pursglove, S.E. and Mackay, J.P.},
title={CSL: A notch above the rest},
journal={International Journal of Biochemistry and Cell Biology},
year={2005},
volume={37},
number={12},
pages={2472-2477},
doi={10.1016/j.biocel.2005.06.013},
note={cited By 28},
url={https://www.scopus.com/inward/record.uri?eid=2-s2.0-25844489960&doi=10.1016%2fj.biocel.2005.06.013&partnerID=40&md5=5acd13aaf52f87227ea36e147dd1b6e6},
affiliation={School of Molecular and Microbial Biosciences, Building G08, University of Sydney, NSW 2006, Australia},
abstract={CSL (CBF1, Suppressor of Hairless, Lag-1) is a transcription factor that is responsible for activating the genes downstream of the Notch signalling pathway, a pathway that is essential for the development of the nervous system and the differentiation of the haematopoietic system among others. In the absence of Notch signalling, CSL represses transcription of Notch target genes, and following activation by Notch, CSL is converted into a transcriptional activator and activates transcription of the same genes. These two opposing functions of CSL are mediated through interactions with distinct protein complexes. The Notch signalling pathway and its crucial cofactor CSL can maintain cells in an undifferentiated state, and have therefore been associated with a growing list of cancers. In addition, CSL has been co-opted by Epstein-Barr virus to mediate viral and host gene transcription following infection. © 2005 Elsevier Ltd. All rights reserved.},
author_keywords={CSL;  Epstein-Barr virus;  Notch;  Suppressor of Hairless;  Transcription},
keywords={Notch receptor;  transcription factor;  transcription factor CSL;  unclassified drug, cancer growth;  cell differentiation;  Epstein Barr virus;  gene activation;  gene repression;  gene targeting;  genetic transcription;  hematopoietic system;  human;  immune response;  nervous system development;  nonhuman;  nucleotide sequence;  protein interaction;  review;  signal transduction;  transcription initiation;  virus infection;  virus transcription, Human herpesvirus 4},
publisher={Elsevier Ltd},
issn={13572725},
coden={IJBBF},
pubmed_id={16095948},
language={English},
abbrev_source_title={Int. J. Biochem. Cell Biol.},
document_type={Short Survey},
source={Scopus},
}

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In the absence of Notch signalling, CSL represses transcription of Notch target genes, and following activation by Notch, CSL is converted into a transcriptional activator and activates transcription of the same genes. These two opposing functions of CSL are mediated through interactions with distinct protein complexes. The Notch signalling pathway and its crucial cofactor CSL can maintain cells in an undifferentiated state, and have therefore been associated with a growing list of cancers. In addition, CSL has been co-opted by Epstein-Barr virus to mediate viral and host gene transcription following infection. © 2005 Elsevier Ltd. 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