Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1-containing complexes

Greenberg, Roger A.; Sobhian, Bijan; Pathania, Shailja; Cantor, Sharon B.; Nakatani, Yoshihiro; Livingston, David M.

doi:10.1101/gad.1381306

Cited by 308DNA Repair MechanismsBRCA gene mutations in cancerPARP inhibition in cancer therapy

Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1-containing complexes

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Greenberg, Roger A., Sobhian, Bijan, Pathania, Shailja, Cantor, Sharon B., Nakatani, Yoshihiro, Livingston, David M.·2006·Genes & Development

DOI 10.1101/gad.1381306PMC PMC1356099

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Abstract

The BRCA1 gene product and its stoichiometric binding partner, BARD1, play a vital role in the cellular response to DNA damage. However, how they acquire specific biochemical functions after DNA damage is poorly understood. Following exposure to genotoxic stress, DNA damage-specific interactions were observed between BRCA1/BARD1 and the DNA damage-response proteins, TopBP1 and Mre11/Rad50/NBS1. Two distinct DNA damage-dependent super complexes emerged; their activation was dependent, in part, on the actions of specific checkpoint kinases, and each super complex contributed to a distinctive aspect of the DNA damage response. The results support a new, multifactorial model that describes how genotoxic stress enables BRCA1 to execute a diverse set of DNA damage-response functions.

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Abraxas, Bach1, and CtIP directly interact with BRCA1 BRCT domains through the pSPxF motif in a phosphorylation-dependent manner, forming mutually exclusive A, B, and C complexes.
“Three proteins, Abraxas (also known as Abra1, FAM175A, CCDC98), Bach1 (also known as Brip1, FancJ) and CtIP (also known as RBBP8), directly interact with the BRCA1 BRCT domains through the pSPxF motif in a phosphorylation-dependent manner forming mutually exclusive complexes, which were thus named as the A, B and C complexes of BRCA1 (Greenberg et al., 2006; Kim et al., 2007; Liu et al., 2007;”
From The BRCA1-Interacting Protein Abraxas Is Required for Genomic Stability and Tumor Suppression (2014) · cites this paper as Greenberg et al., 2006
FANCJ helicase activity induced in S phase is required for FANCJ to promote S phase progression and possibly intra-S phase checkpoints.
“FANCJ helicase activity induced in S phase is also required for FANCJ to promote S phase progression and possibly intra-S phase checkpoints [71,72].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [72]

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Authors: Greenberg, R. A., Sobhian, B., Pathania, S., Cantor, S. B., Nakatani, Y., & Livingston, D. M.
Affiliations: Harvard University (US)
ORCID: Greenberg, Roger A.
Sobhian, Bijan
Pathania, Shailja
Cantor, Sharon B.
Livingston, David M.
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 2006-01-01
Volume: 20
Issue: 1
Pages: 34-46
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.1381306
PMC: PMC1356099
OpenAlex: W2164458581
Cited by: 308
References: 61
Citations by year: 2026: 2 · 2025: 3 · 2024: 4 · 2023: 9 · 2022: 12 · 2021: 17 · 2020: 13 · 2019: 4 · 2018: 14 · 2017: 12 · 2016: 10 · 2015: 19 · 2014: 21 · 2013: 19 · 2012: 22
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
eScholarship@UMassChan (submittedVersion)
Funders: Leukemia Research Foundation
Broad Institute
Österreichischen Akademie der Wissenschaften
National Cancer Institute
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, BARD1, DNA damage response, TopBP1, Mre11-Rad50-Nbs1, checkpoint kinase, genotoxic stress
MeSH terms: MRE11 Homologue Protein, Carrier Proteins, Cell Cycle, DNA Damage, DNA Repair, DNA-Binding Proteins, Humans, Nuclear Proteins, Protein Binding, Acid Anhydride Hydrolases, Cell Cycle Proteins, BRCA1 Protein, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases, DNA Repair Enzymes, Cell Line, Tumor

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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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Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1-containing complexes

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