期刊
TRENDS IN GENETICS
卷 37, 期 11, 页码 973-985出版社
CELL PRESS
DOI: 10.1016/j.tig.2021.06.010
关键词
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资金
- Institut Curie
- INSERM
- ANR [ANR-19-CE12-0016-03]
- Ligue contre le cancer Equipe Labellisee 2020 (EL2020LNCC/Sal)
- Fondation ARC
- French governmental fellowship
- CNRS
- Agence Nationale de la Recherche (ANR) [ANR-19-CE12-0016] Funding Source: Agence Nationale de la Recherche (ANR)
RNAs and associated proteins, including RNA binding proteins, may regulate NHEJ during DNA replication to sustain genome stability.
Defective DNA replication, known as 'replication stress', is a source of DNA damage, a hallmark of numerous human diseases, including cancer, developmental defect, neurological disorders, and premature aging. Recent work indicates that non-homologous end-joining (NHEJ) is unexpectedly active during DNA replication to repair replication-born DNA lesions and to safeguard replication fork integrity. However, erroneous NHEJ events are deleterious to genome stability. RNAs are novel regulators of NHEJ activity through their ability to modulate the assembly of repair complexes in trans. At DNA damage sites, RNAs and DNA-embedded ribonucleotides modulate repair efficiency and fidelity. We discuss here how RNAs and associated proteins, including RNA binding proteins, may regulate NHEJ to sustain genome stability during DNA replication.
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