Regulation of DNA damage recognition and nucleotide excision repair: another role for p53.
In response to DNA damage, the p53 tumor suppressor gene product is activated leading to the induction of several downstream cellular processes including cell cycle checkpoints, DNA repair or apoptosis. Experiments first performed in the Hanawalt laboratory identified a p53-dependent pathway affecting global genomic nucleotide excision repair. The mechanisms involved in this process include both transcriptional and post-translational regulation by p53 of the DDB2 and XPC gene products, two critical DNA damage recognition proteins required for GGR. A historical review of this work is presented.
Ford
James M
JM
Department of Medicine (Oncology), Stanford University School of Medicine, 1115 CCSR Bldg., 269 Campus Drive Stanford, CA 94305, USA. jmf@stanford.edu
D004249:DNA Damage; D004260:DNA Repair / Q000235:genetics; D004268:DNA-Binding Proteins / Q000502:physiology; D011499:Protein Processing, Post-Translational; D012323:RNA Processing, Post-Transcriptional; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
C117669:DDB2 protein, human; D004268:DNA-Binding Proteins; D016159:Tumor Suppressor Protein p53