ArticleEMBO reports2016
53BP1 ablation rescues genomic instability in mice expressing 'RING-less' BRCA1.
Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 48 citations in OpenAlex.
- 53BP1-independent Shieldin-BRCA1 antagonism at replication-coupled double-strand breaks.Nature communications · 2026Article
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.Nature structural & molecular biology · 2025Article
- Article
- The chromatin-associated 53BP1 ortholog, HSR-9, regulates recombinational repair andbioRxiv : the preprint server for biology · 2024Article
- Brca1 Mouse Models: Functional Insights and Therapeutic Opportunities.Journal of molecular biology · 2024Review
- How to sensitize glioblastomas to temozolomide chemotherapy: a gap-centered view.Frontiers in cell and developmental biology · 2024Review
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.bioRxiv : the preprint server for biology · 2023Article
- Mechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting.Nature communications · 2023Article
- BRCA1 the Versatile Defender: Molecular to Environmental Perspectives.International journal of molecular sciences · 2023Review
- The Tumor Suppressor BRCA1/2, Cancer Susceptibility and Genome Instability in Gynecological and Mammary Cancers.Asian Pacific journal of cancer prevention : APJCP · 2023Review
- Differential requirement for BRCA1-BARD1 E3 ubiquitin ligase activity in DNA damage repair and meiosis in the Caenorhabditis elegans germ line.PLoS genetics · 2023Article
- Article
- Autologous K63 deubiquitylation within the BRCA1-A complex licenses DNA damage recognition.The Journal of cell biology · 2022Article
- ATR/ATM-Mediated Phosphorylation of BRCA1 T1394 Promotes Homologous Recombinational Repair and GCancer research · 2021Article
- Is it a wrap? Nucleosome interactions of the BRCA1-binding partner, BARD1, steal the scene.Nature structural & molecular biology · 2021Article
- RNF168-mediated localization of BARD1 recruits the BRCA1-PALB2 complex to DNA damage.Nature communications · 2021Article
- 53BP1 loss rescues embryonic lethality but not genomic instability of BRCA1 total knockout mice.Cell death and differentiation · 2020Article
- The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication.Nature reviews. Molecular cell biology · 2020Review
- 53BP1 Enforces Distinct Pre- and Post-resection Blocks on Homologous Recombination.Molecular cell · 2020Article
- BRCA1 and homologous recombination: implications from mouse embryonic development.Cell & bioscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
BRCA1 mutations strongly predispose affected individuals to breast and ovarian cancer, but the mechanism by which BRCA1 acts as a tumor suppressor is not fully understood. Homozygous deletion of exon 2 of the mouse Brca1 gene normally causes embryonic lethality, but we show that exon 2-deleted alleles of Brca1 are expressed as a mutant isoform that lacks the N-terminal RING domain. This "RING-less" BRCA1 protein is stable and efficiently recruited to the sites of DNA damage. Surprisingly, robust RAD51 foci form in cells expressing RING-less BRCA1 in response to DNA damage, but the cells nonetheless display the substantial genomic instability. Genomic instability can be rescued by the deletion of Trp53bp1, which encodes the DNA damage response factor 53BP1, and mice expressing RING-less BRCA1 do not show an increased susceptibility to tumors in the absence of 53BP1. Genomic instability in cells expressing RING-less BRCA1 correlates with the loss of BARD1 and a defect in restart of replication forks after hydroxyurea treatment, suggesting a role of BRCA1-BARD1 in genomic integrity that is independent of RAD51 loading.
Indexed as
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.