DNA damage signaling recruits the RNA polymerase II binding protein Che-1 to the p53 promoter.
New work by Bruno et al. (2006) describes a mechanistic switch of the proliferation-promoting Che-1 activator of E2F-target genes into a cell-cycle inhibitor in response to DNA damage, through Che-1 relocalization to, and activation of, the p53 tumor suppressor gene.
Halazonetis
Thanos D
TD
Department of Molecular Biology, University of Geneva, CH-1211, Geneva 4, Switzerland.
Bartek
Jiri
J
D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004249:DNA Damage; D006801:Humans; D008954:Models, Biological; D010750:Phosphoproteins / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D012097:Repressor Proteins / Q000378:metabolism*; D015398:Signal Transduction; D014157:Transcription Factors / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
C402637:AATF protein, human; D051017:Apoptosis Regulatory Proteins; C493956:CDKN1A protein, human; D002352:Carrier Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D010750:Phosphoproteins; C046282:RNA polymerase II-binding proteins; D012097:Repressor Proteins; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53