| Autor: |
Nieto Moreno N; Department of Cellular and Molecular Medicine, Panum Institute, University of Copenhagen, Copenhagen, Denmark; email: jsvejstrup@sund.ku.dk., Olthof AM; Department of Cellular and Molecular Medicine, Panum Institute, University of Copenhagen, Copenhagen, Denmark; email: jsvejstrup@sund.ku.dk., Svejstrup JQ; Department of Cellular and Molecular Medicine, Panum Institute, University of Copenhagen, Copenhagen, Denmark; email: jsvejstrup@sund.ku.dk.; Mechanisms of Transcription Laboratory, The Francis Crick Institute, London, United Kingdom. |
| Jazyk: |
angličtina |
| Zdroj: |
Annual review of biochemistry [Annu Rev Biochem] 2023 Jun 20; Vol. 92, pp. 81-113. Date of Electronic Publication: 2023 Apr 11. |
| DOI: |
10.1146/annurev-biochem-052621-091205 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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