@article {HARDY2483, author = {TABITHA M. HARDY and MA SURESH KUMAR and MARTIN L. SMITH}, title = {RB Stabilizes XPC and Promotes Cellular NER}, volume = {30}, number = {7}, pages = {2483--2488}, year = {2010}, publisher = {International Institute of Anticancer Research}, abstract = {It has long been thought that the G1/S cell cycle checkpoint allows time for DNA repair by delaying S-phase entry. The p53 tumor suppressor pathway regulates the G1/S checkpoint by regulating the cyclin-dependent kinase inhibitor p21Waf1/Cip1, but p53 also regulates the nucleotide excision DNA repair protein XPC. Here, using p53-null cell lines we show that additional mechanisms stabilize XPC protein and promote nucleotide excision repair (NER) in concert with the G1/S checkpoint. At least one mechanism to stabilize and destabilize XPC involves ubiquitin-mediated degradation of XPC, as the ubiquitin ligase inhibitor MG-132 blocked XPC degradation. The retinoblastoma protein RB, in its unphosphorylated form actually stabilized XPC and promoted NER as measured by host cell reactivation experiments. The data suggest that XPC protein and XPC-mediated NER are tightly linked to the G1/S checkpoint, even in cells lacking functional p53.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/30/7/2483}, eprint = {https://ar.iiarjournals.org/content/30/7/2483.full.pdf}, journal = {Anticancer Research} }