Document Detail


AP-1 in cell proliferation and survival.
MedLine Citation:
PMID:  11402335     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A plethora of physiological and pathological stimuli induce and activate a group of DNA binding proteins that form AP-1 dimers. These proteins include the Jun, Fos and ATF subgroups of transcription factors. Recent studies using cells and mice deficient in individual AP-1 proteins have begun to shed light on their physiological functions in the control of cell proliferation, neoplastic transformation and apoptosis. Above all such studies have identified some of the target genes that mediate the effects of AP-1 proteins on cell proliferation and death. There is evidence that AP-1 proteins, mostly those that belong to the Jun group, control cell life and death through their ability to regulate the expression and function of cell cycle regulators such as Cyclin D1, p53, p21(cip1/waf1), p19(ARF) and p16. Amongst the Jun proteins, c-Jun is unique in its ability to positively regulate cell proliferation through the repression of tumor suppressor gene expression and function, and induction of cyclin D1 transcription. These actions are antagonized by JunB, which upregulates tumor suppressor genes and represses cyclin D1. An especially important target for AP-1 effects on cell life and death is the tumor suppressor p53, whose expression as well as transcriptional activity, are modulated by AP-1 proteins.
Authors:
E Shaulian; M Karin
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Oncogene     Volume:  20     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  2001 Apr 
Date Detail:
Created Date:  2001-06-12     Completed Date:  2001-07-05     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  2390-400     Citation Subset:  IM    
Affiliation:
Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California San Diego, 9500 Gilman Drive, La Jolla, California, CA 92093-0636, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Cell Cycle Proteins / biosynthesis,  genetics
Cell Division
Cell Survival
Cell Transformation, Neoplastic
Mice
Models, Biological
Signal Transduction
Transcription Factor AP-1 / physiology*
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Transcription Factor AP-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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