Cited by 1,245DNA Repair MechanismsBRCA gene mutations in cancerPARP inhibition in cancer therapy

The DOI matches its Crossref record; 52 of the 60 references it cites were found in a registry or an index.

Brca1 Controls Homology-Directed DNA Repair

Open access

Abstract

Germline mutations in BRCA1 confer a high risk of breast and ovarian tumors. The role of BRCA1 in tumor suppression is not yet understood, but both transcription and repair functions have been ascribed. Evidence that BRCA1 is involved in DNA repair stems from its association with RAD51, a homolog of the yeast protein involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination. We report here that Brca1-deficient mouse embryonic stem cells have impaired repair of chromosomal DSBs by homologous recombination. The relative frequencies of homologous and nonhomologous DNA integration and DSB repair were also altered. The results demonstrate a caretaker role for BRCA1 in preserving genomic integrity by promoting homologous recombination and limiting mutagenic nonhomologous repair processes.

Overview

Integrity signals

Registry

Crossref · 10.1016/s1097-2765(00)80202-6

Cites

52 of 52 references verified0 citation errors · 0 not checkable

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Claims the paper makes

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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The BRCA1-BARD1 complex acts in homologous recombination-mediated repair of DNA double-strand breaks.

    “The tumor suppressor complex BRCA1-BARD1 functions in DNA double-strand break repair by homologous recombination.”

    From BRCA1–BARD1 promotes RAD51-mediated homologous DNA pairing (2017) · cites this paper as [18]

Citations

Cites

3 retracted

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8 of the 60 references couldn’t be matched to a known paper.

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Metadata

Authors
Moynahan, M. E., Chiu, J. W., Koller, B. H., & Jasin, M.
Affiliations
  • Memorial Sloan Kettering Cancer Center (US)
  • University of North Carolina at Chapel Hill (US)
Corresponding author
Jasin, Maria
Venue
Molecular Cell
Publisher
Elsevier BV
Published
1999-10
Volume
4
Issue
4
Pages
511-518
ISSN
1097-2765 (ISSN-L)
OpenAlex
W2059365987
Cited by
1,245
References
60
Citations by year
2026: 27 · 2025: 18 · 2024: 22 · 2023: 35 · 2022: 21 · 2021: 42 · 2020: 47 · 2019: 48 · 2018: 53 · 2017: 47 · 2016: 47 · 2015: 45 · 2014: 55 · 2013: 58 · 2012: 47
FWCI
22.97
Type
journal article
Language
en
Open access
Locations
  • Molecular Cell (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
  • UNC Libraries
Funders
  • National Institutes of Health
  • National Cancer Institute (1P50CA68425, P50CA068425)
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, homologous recombination, homology-directed repair, DNA double-strand break repair, RAD51, non-homologous end joining, genome stability, tumor suppression, mouse embryonic stem cells, germline mutations, breast and ovarian cancer
MeSH terms
Animals, Arabinofuranosyluracil, Cell Line, Chromosomes, DNA Damage, DNA Repair, DNA-Binding Proteins, Mutation, Proto-Oncogene Proteins, Recombination, Genetic, Stem Cells, Thymidine Kinase, Transfection, Retinoblastoma Protein, Mice, Knockout, Gene Targeting, BRCA1 Protein, Rad51 Recombinase, Mice

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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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