期刊
ANNUAL REVIEW OF BIOCHEMISTRY, VOL 88
卷 88, 期 -, 页码 221-245出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-biochem-013118-111058
关键词
homologous recombination; DNA damage repair; replication fork repair; replication fork protection; genome maintenance; BRCA1; BARD1; BRCA2; tumor suppression
资金
- NCI NIH HHS [R01 CA205224, P01 CA092584, P30 CA054174, R01 CA220123] Funding Source: Medline
- NIEHS NIH HHS [R01 ES021454, R01 ES007061] Funding Source: Medline
- NIGMS NIH HHS [R01 GM109645] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA092584, R01CA220123, P30CA054174, R01CA205224] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES007061] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM109645] Funding Source: NIH RePORTER
Mutations in the BRCA1 and BRCA2 genes predispose afflicted individuals to breast, ovarian, and other cancers. The BRCA-encoded products form complexes with other tumor suppressor proteins and with the recombinase enzyme RAD51 to mediate chromosome damage repair by homologous recombination and also to protect stressed DNA replication forks against spurious nucleolytic attrition. Understanding how the BRCA tumor suppressor network executes its biological functions would provide the foundation for developing targeted cancer therapeutics, but progress in this area has been greatly hampered by the challenge of obtaining purified BRCA complexes for mechanistic studies. In this article, we review how recent effort begins to overcome this technical challenge, leading to functional and structural insights into the biochemical attributes of these complexes and the multifaceted roles that they fulfill in genome maintenance. We also highlight the major mechanistic questions that remain.
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