Regulation of DNA damage response pathways by the cullin-RING ubiquitin ligases.
Eukaryotic cells repair ultraviolet light (UV)- and chemical carcinogen-induced DNA strand-distorting damage through the nucleotide excision repair (NER) pathway. Concurrent activation of the DNA damage checkpoints is also required to arrest the cell cycle and allow time for NER action. Recent studies uncovered critical roles for ubiquitin-mediated post-translational modifications in controlling both NER and checkpoint functions. In this review, we will discuss recent progress in delineating the roles of cullin-RING E3 ubiquitin ligases in orchestrating the cellular DNA damage response through ubiquitination of NER factors, histones, and checkpoint effectors.
Hannah
Jeffrey
J
Department of Pathology and Laboratory Medicine, Weill Cornell Medical College and Weill Cornell Graduate School of Medical Sciences, 1300 York Avenue, New York, NY 10065, United States.
Zhou
Pengbo
P
D000818:Animals; D002273:Carcinogens / Q000633:toxicity; D002453:Cell Cycle; D004247:DNA / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D004249:DNA Damage / Q000187:drug effects / Q000528:radiation effects; D004260:DNA Repair; D005057:Eukaryotic Cells / Q000166:cytology; D018816:Genes, cdc; D006657:Histones / Q000378:metabolism; D006801:Humans; D054829:RING Finger Domains; D044843:SKP Cullin F-Box Protein Ligases / Q000737:chemistry / Q000502:physiology; D054875:Ubiquitination; D014466:Ultraviolet Rays
D002273:Carcinogens; D006657:Histones; D004247:DNA; D044843:SKP Cullin F-Box Protein Ligases