ArticleCancer research2015
Repair versus Checkpoint Functions of BRCA1 Are Differentially Regulated by Site of Chromatin Binding.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- A ubiquitin chain-feeding mechanism for BRCA1-A.Nature communications · 2026Article
- Identification of Hub Genes for Psoriasis and Cancer by Bioinformatic Analysis.BioMed research international · 2024Article
- WWOX binds MERIT40 and modulates its function in homologous recombination, implications in breast cancer.Cancer gene therapy · 2023Article
- Structural and Functional Basis of JAMM Deubiquitinating Enzymes in Disease.Biomolecules · 2022Review
- Glycogen synthase kinase 3β inhibition synergizes with PARP inhibitors through the induction of homologous recombination deficiency in colorectal cancer.Cell death & disease · 2021Article
- Review
- Review
- RAP80 and BRCA1 PARsylation protect chromosome integrity by preventing retention of BRCA1-B/C complexes in DNA repair foci.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- PDA Indolylmaleimides Induce Anti-Tumor Effects in Prostate Carcinoma Cell Lines Through Mitotic Death.Frontiers in veterinary science · 2020Article
- The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage.Aging · 2019Article
- Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation.Molecular cell · 2019Article
- The Cajal Body Protein WRAP53β Prepares the Scene for Repair of DNA Double-Strand Breaks by Regulating Local Ubiquitination.Frontiers in molecular biosciences · 2019Review
- Clinical and Biological Manifestation of RNF168 Deficiency in Two Polish Siblings.Frontiers in immunology · 2017Article
- HP1 regulates the localization of FANCJ at sites of DNA double-strand breaks.Cancer science · 2016Article
- Opposing roles of RNF8/RNF168 and deubiquitinating enzymes in ubiquitination-dependent DNA double-strand break response signaling and DNA-repair pathway choice.Journal of radiation research · 2016Review
- Analogs of the novel phytohormone, strigolactone, trigger apoptosis and synergize with PARP inhibitors by inducing DNA damage and inhibiting DNA repair.Oncotarget · 2016Article
- ATM Dependent Silencing Links Nucleolar Chromatin Reorganization to DNA Damage Recognition.Cell reports · 2015Article
- MERIT40 cooperates with BRCA2 to resolve DNA interstrand cross-links.Genes & development · 2015Article
- Deciphering the BRCA1 Tumor Suppressor Network.The Journal of biological chemistry · 2015Review
- Fine-tuning the ubiquitin code at DNA double-strand breaks: deubiquitinating enzymes at work.Frontiers in genetics · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The product of the Brca1 tumor-suppressor gene is involved in multiple aspects of the cellular DNA damage response (DDR), including activation of cell-cycle arrests and DNA double-stranded break (DSB) repair by homologous recombination. Prior reports demonstrated that BRCA1 recruitment to areas of DNA breakage depended on RAP80 and the RNF8/RNF168 E3 ubiquitin ligases. Here, we extend these findings by showing that RAP80 is only required for the binding of BRCA1 to regions flanking the DSB, whereas BRCA1 binding directly to DNA breaks requires Nijmegen breakage syndrome 1 (NBS1). These differential recruitment mechanisms differentially affect BRCA1 functions: (i) RAP80-dependent recruitment of BRCA1 to chromatin flanking DNA breaks is required for BRCA1 phosphorylation at serine 1387 and 1423 by ATM and, consequently, for the activation of S and G(2) checkpoints; and (ii) BRCA1 interaction with NBS1 upon DSB induction results in an NBS1-dependent recruitment of BRCA1 directly to the DNA break and is required for nonhomologous end-joining repair. Together, these findings illustrate that spatially distinct fractions of BRCA1 exist at the DSB site, which are recruited by different mechanisms and execute different functions in the DDR.
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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.