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.
View details for DOI 10.1016/j.mrfmmm.2005.04.005
View details for Web of Science ID 000231164900016
View details for PubMedID 15927209