核苷酸切除修复
Cockayne综合征
色素性干皮病
DNA修复
DNA损伤
生物
抄写(语言学)
遗传学
细胞生物学
DNA
RNA聚合酶Ⅱ
分子生物学
基因
基因表达
发起人
语言学
哲学
作者
Nicolás Nieto Moreno,Anouk M Olthof,Jesper Q. Svejstrup
标识
DOI:10.1146/annurev-biochem-052621-091205
摘要
Ultraviolet (UV) irradiation and other genotoxic stresses induce bulky DNA lesions, which threaten genome stability and cell viability. Cells have evolved two main repair pathways to remove such lesions: global genome nucleotide excision repair (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER). The modes by which these subpathways recognize DNA lesions are distinct, but they converge onto the same downstream steps for DNA repair. Here, we first summarize the current understanding of these repair mechanisms, specifically focusing on the roles of stalled RNA polymerase II, Cockayne syndrome protein B (CSB), CSA and UV-stimulated scaffold protein A (UVSSA) in TC-NER. We also discuss the intriguing role of protein ubiquitylation in this process. Additionally, we highlight key aspects of the effect of UV irradiation on transcription and describe the role of signaling cascades in orchestrating this response. Finally, we describe the pathogenic mechanisms underlying xeroderma pigmentosum and Cockayne syndrome, the two main diseases linked to mutations in NER factors.
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