ArticleJournal of nucleic acids2010
BRCA1 Forms a Functional Complex with γ-H2AX as a Late Response to Genotoxic Stress.
Article in Journal of nucleic acids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Coincidence of L1 retrotransposition and DNA repair deficiency elicits synthetic lethality in S-phase mature neurons.iScience · 2026Article
- Review
- Compensation for X-linked Pdha1 silencing by Pdha2 is essential for meiotic double-strand break repair in spermatogenesis.Development (Cambridge, England) · 2025Article
- Article
- Defective Homologous Recombination Repair By Up-Regulating Lnc-HZ10/Ahr Loop in Human Trophoblast Cells Induced Miscarriage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- BRCA1 interactors, RAD50 and BRIP1, as prognostic markers for triple-negative breast cancer severity.Frontiers in genetics · 2023Article
- BRCA1 haploinsufficiency promotes chromosomal amplification under Fenton reaction-based carcinogenesis through ferroptosis-resistance.Redox biology · 2022Article
- Modulation of BRCA1 mediated DNA damage repair by deregulated ER-α signaling in breast cancers.American journal of cancer research · 2022Article
- LEDGF/p75 Is Required for an Efficient DNA Damage Response.International journal of molecular sciences · 2021Article
- countfitteR: efficient selection of count distributions to assess DNA damage.Annals of translational medicine · 2021Article
- Mortaparib, a novel dual inhibitor of mortalin and PARP1, is a potential drug candidate for ovarian and cervical cancers.Journal of experimental & clinical cancer research : CR · 2019Article
- Perturbation of PALB2 function by the T413S mutation found in small cell lung cancer.Wellcome open research · 2017Article
- A p53 axis regulates B cell receptor-triggered, innate immune system-driven B cell clonal expansion.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Roles of Kruppel-associated Box (KRAB)-associated Co-repressor KAP1 Ser-473 Phosphorylation in DNA Damage Response.The Journal of biological chemistry · 2012Article
- Central Role of Ubiquitination in Genome Maintenance: DNA Replication and Damage Repair.ISRN molecular biology · 2012Review
- Oncogenic RAS regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence.Developmental cell · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Following genotoxic stress, the histone H2AX becomes phosphorylated at serine 139 by the ATM/ATR family of kinases. The tumor suppressor BRCA1, also phosphorylated by ATM/ATR kinases, is one of several proteins that colocalize with phospho-H2AX (γ-H2AX) at sites of active DNA repair. Both the precise mechanism and the purpose of BRCA1 recruitment to sites of DNA damage are unknown. Here we show that BRCA1 and γ-H2AX form an acid-stable biochemical complex on chromatin after DNA damage. Maximal association of BRCA1 with γ-H2AX correlates with reduced global γ-H2AX levels on chromatin late in the repair process. Since BRCA1 is known to have E3 ubiquitin ligase activity in vitro, we examined H2AX for evidence of ubiquitination. We found that H2AX is ubiquitinated at lysines 119 and 119 in vivo and that blockage of 26S proteasome function stabilizes γ-H2AX levels within cells. When BRCA1 levels were reduced, ubiquitination of H2AX was also reduced, and the cells retained higher levels of phosphorylated H2AX. These results indicate that BRCA1 is recruited into stable complexes with γ-H2AX and that the complex is involved in attenuation of the γ-H2AX repair signal after DNA damage.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.