Regulation of damage recognition in mammalian global genomic nucleotide excision repair.
Nucleotide excision repair operating throughout the mammalian genome plays a crucial role in the suppression of mutagenesis and carcinogenesis, which can arise from DNA lesions induced by a wide variety of genotoxic agents, such as ultraviolet light and chemical compounds. A key process of this DNA repair pathway, damage recognition, is accomplished through multiple steps including concerted actions of the damaged DNA binding factors XPC and UV-DDB, both of which are implicated in a human cancer-prone genetic disorder, xeroderma pigmentosum. Accumulating evidence indicates that the expression and functions of these damage recognition factors are subject to exquisite regulation at diverse levels, including transcriptional activation, post-translational modification, complex formation, and protein degradation through ubiquitination.
Sugasawa
Kaoru
K
Biosignal Research Center, Organization of Advanced Science and Technology, Kobe University, Kobe, Hyogo 657-8501, Japan. ksugasawa@garnet.kobe-u.ac.jp
D000818:Animals; D044842:Cullin Proteins / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D008957:Models, Genetic; D054875:Ubiquitination
C114234:CUL4A protein, human; D044842:Cullin Proteins; C117669:DDB2 protein, human; D004268:DNA-Binding Proteins; C086984:XPC protein, human