The role of BRCA1 in DNA damage response
Open accessAbstract
BRCA1 is a well-established tumor suppressor gene, which is frequently mutated in familial breast and ovarian cancers. The gene product of BRCA1 functions in a number of cellular pathways that maintain genomic stability, including DNA damage-induced cell cycle checkpoint activation, DNA damage repair, protein ubiquitination, chromatin remodeling, as well as transcriptional regulation and apoptosis. In this review, we discuss recent advances regarding our understanding of the role of BRCA1 in tumor suppression and DNA damage response, including DNA damage-induced cell cycle checkpoint activation and DNA damage repair.
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BRCA1 may be a key player in the DNA damage response.
“Evidence suggests that BRCA1 could be one of the key players in DNA damage response [281].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [281]
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Impacts of Cancer-associated Mutations on the Structure–Activity Relationship of BAP1
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Evaluation of antitumoral effect of Hibiscus sabdariffa extract on human breast cancer cells
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Polθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours
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- Authors
- Wu, J., Lu, L.-Y., & Yu, X.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Yu, Xiaochun
- Venue
- Protein & Cell
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-02
- Volume
- 1
- Issue
- 2
- Pages
- 117-123
- ISSN
- 1674-800X (ISSN-L)
- 1674-8018
- PMC
- PMC3078634
- OpenAlex
- W2140930673
- Cited by
- 235
- References
- 100
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 25 · 2023: 17 · 2022: 32 · 2021: 20 · 2020: 15 · 2019: 18 · 2018: 16 · 2017: 9 · 2016: 15 · 2015: 9 · 2014: 13 · 2013: 15 · 2012: 9
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Protein & Cell (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Michigan
- National Institutes of Health
- National Cancer Institute (R01CA132755, R01CA130899, CA132755)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- BRCA1, DNA damage response, tumor suppression, DNA repair, genome stability, ubiquitination, chromatin remodeling, transcriptional regulation, apoptosis, breast cancer, ovarian cancer
- MeSH terms
- Breast Neoplasms, DNA Damage, DNA Repair, Female, Humans, Mutation, Ovarian Neoplasms, Signal Transduction, Genes, Tumor Suppressor, Apoptosis, Genes, cdc, BRCA1 Protein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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