ArticleCell cycle (Georgetown, Tex.)2015
Damage-induced BRCA1 phosphorylation by Chk2 contributes to the timing of end resection.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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
27 citing papers in PubMed.
- Article
- Article
- Targeting the Cdc2-like kinase 2 for overcoming platinum resistance in ovarian cancer.MedComm · 2024Article
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- Phosphorylation of BRCA1 by ATM upon double-strand breaks impacts ATM function in end-resection: A potential feedback loop.iScience · 2022Article
- Wwox Binding to the Murine Brca1-BRCT Domain Regulates Timing of Brip1 and CtIP Phospho-Protein Interactions with This Domain at DNA Double-Strand Breaks, and Repair Pathway Choice.International journal of molecular sciences · 2022Article
- Functional Analysis Identifies Damaging CHEK2 Missense Variants Associated with Increased Cancer Risk.Cancer research · 2022Article
- Modulation of BRCA1 mediated DNA damage repair by deregulated ER-α signaling in breast cancers.American journal of cancer research · 2022Article
- USP39 promotes non-homologous end-joining repair by poly(ADP-ribose)-induced liquid demixing.Nucleic acids research · 2021Article
- Proteins from the DNA Damage Response: Regulation, Dysfunction, and Anticancer Strategies.Cancers · 2021Review
- BRCA1 Antibodies Matter.International journal of biological sciences · 2021Article
- Inactivation of the Prolyl Isomerase Pin1 Sensitizes BRCA1-Proficient Breast Cancer to PARP Inhibition.Cancer research · 2020Article
- The F-Box-Like Protein FBL17 Is a Regulator of DNA-Damage Response and Colocalizes with RETINOBLASTOMA RELATED1 at DNA Lesion Sites.Plant physiology · 2020Article
- The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage.Aging · 2019Article
- Correlation of homologous recombination deficiency induced mutational signatures with sensitivity to PARP inhibitors and cytotoxic agents.Genome biology · 2019Article
- Mapping genetic interactions in cancer: a road to rational combination therapies.Genome medicine · 2019Review
- MiR223-3p promotes synthetic lethality in BRCA1-deficient cancers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells.Toxicology research · 2019Article
- Article
- DNA-damage-induced degradation of EXO1 exonuclease limits DNA end resection to ensure accurate DNA repair.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
The BRCA1 tumor suppressor plays an important role in homologous recombination (HR)-mediated DNA double-strand-break (DSB) repair. BRCA1 is phosphorylated by Chk2 kinase upon γ-irradiation, but the role of Chk2 phosphorylation is not understood. Here, we report that abrogation of Chk2 phosphorylation on BRCA1 delays end resection and the dispersion of BRCA1 from DSBs but does not affect the assembly of Mre11/Rad50/NBS1 (MRN) and CtIP at DSBs. Moreover, we show that BRCA1 is ubiquitinated by SCF(Skp2) and that abrogation of Chk2 phosphorylation impairs its ubiquitination. Our study suggests that BRCA1 is more than a scaffold protein to assemble HR repair proteins at DSBs, but that Chk2 phosphorylation of BRCA1 also serves as a built-in clock for HR repair of DSBs. BRCA1 is known to inhibit Mre11 nuclease activity. SCF(Skp2) activity appears at late G1 and peaks at S/G2, and is known to ubiquitinate phosphodegron motifs. The removal of BRCA1 from DSBs by SCF(Skp2)-mediated degradation terminates BRCA1-mediated inhibition of Mre11 nuclease activity, allowing for end resection and restricting the initiation of HR to the S/G2 phases of the cell cycle.
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