期刊
ANNUAL REVIEW OF GENETICS
卷 43, 期 -, 页码 223-249出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-genet-102108-134222
关键词
DNA repair; interstrand crosslink; cancer; homologous recombination; translesion synthesis; protein ubiquitination
资金
- NIH [RO1DK43889, RO1HL52725, PO1DK50654, U19A1067751, 5PO1CA092584]
- International Human Frontiers Science Program Organization
- NATIONAL CANCER INSTITUTE [P01CA092584] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL052725, R37HL052725] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI067751] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK050654, R01DK043889] Funding Source: NIH RePORTER
Fanconi Anemia (FA) is an inherited genomic instability disorder, caused by mutations in genes regulating replication-dependent removal of interstrand DTNA crosslinks. The Fanconi Anemia pathway is thought to coordinate a complex mechanism that enlists elements of three classic DNA repair pathways, namely homologous recombination, nucleotide excision repair, and mutagenic translesion synthesis, in response to genotoxic insults. To this end, the Fanconi Anemia pathway employs a unique nuclear protein complex that ubiquitinates FANCD2 and FANCI, leading to formation of DNA repair structures. Lack of obvious enzymatic activities among most FA members has made it challenging to unravel its precise modus operandi. Here we review the current understanding of how the Fanconi Anemia pathway components participate in DNA repair and discuss the mechanisms that regulate this pathway to ensure timely, efficient, and correct restoration of chromosomal integrity.
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