ArticleThe Journal of biological chemistry2013
RIF1 counteracts BRCA1-mediated end resection during DNA repair.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers.
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Who cites it
184 citing papers in PubMed, 272 citations in OpenAlex.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- HP1β recruits RING1A to ubiquitinate histone H2A for BRCA1-mediated resection of double-stand breaks.iScience · 2026Article
- ATM Inhibition Enhances Knock-in Efficiency by Suppressing AAV-Induced Activation of Apoptotic Pathways.Communications biology · 2026Article
- Daxx-Dependent H3.3 Deposition Promotes Double-Strand Breaks Repair by Homologous Recombination.Cells · 2026Article
- Recombination junctions from antibody isotype switching classify immune and DNA repair dysfunction.Nature communications · 2025Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Comprehensive assessment of homologous recombination deficiency via simultaneous methylation and mutation analysis in epithelial ovarian cancer: implications for PARP inhibitors efficacy.Biomarker research · 2025Article
- Profiling BRCA1-BRCT interactions and their functional relevance at amino acid resolution.Nucleic acids research · 2025Article
- USP37 counteracts HLTF to protect damaged replication forks and promote survival of BRCA1-deficient cells and PARP inhibitor resistance.Nucleic acids research · 2025Article
- Nuclear deformability increases PARPi sensitivity in BRCA1-deficient cells by increasing microtubule-dependent DNA break mobility.Nature communications · 2025Article
- Reversible and effective cell cycle synchronization method for studying stage-specific processes.Life science alliance · 2025Article
- Review
- Tousled-like kinase loss confers PARP inhibitor resistance in BRCA1-mutated cancers by impeding non-homologous end joining repair.Molecular medicine (Cambridge, Mass.) · 2025Article
- RIF1 integrates DNA repair and transcriptional requirements during the establishment of humoral immune responses.Nature communications · 2025Article
- BRCA1 and BRCA2: from cancer susceptibility to synthetic lethality.Genes & development · 2025Review
- 53BP1 loss elicits cGAS-STING-dependent antitumor immunity in ovarian and pancreatic cancer.Nature communications · 2024Article
- UBE2D3 facilitates NHEJ by orchestrating ATM signalling through multi-level control of RNF168.Nature communications · 2024Article
- PTEN-mediated dephosphorylation of 53BP1 confers cellular resistance to DNA damage in cancer cells.Molecular oncology · 2024Article
- Rapid evolution of genes with anti-cancer functions during the origins of large bodies and cancer resistance in elephants.bioRxiv : the preprint server for biology · 2024Article
124 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
BRCA1 promotes homologous recombination repair and antagonizes 53BP1-dependent nonhomologous end joining (NHEJ) pathway. However, the molecular basis of the competition between BRCA1 and 53BP1 pathways remains elusive. Here we report that RIF1 protein translocates to damage sites via ATM-dependent 53BP1 phosphorylation. Strikingly, loss of RIF1 rescues initial DNA end resection and checkpoint activation in BRCA1-depleted cells. Interestingly RIF1 accumulation at damage sites is antagonized by BRCA1 in S and G2 phases. Conversely, the translocation of BRCA1 to damage sites is inhibited by RIF1 in G1 phase. However, loss of RIF1 differs from that of 53BP1 deficiency, as it cannot fully rescue RAD51 foci formation, homologous recombination defect, and radio-hypersensitivity in BRCA1-deficient cells. This is likely because RIF1, but not 53BP1, also regulates the foci formation and chromatin loading of BLM (the Bloom syndrome helicase). Thus, RIF1 not only acts downstream of 53BP1 and counteracts BRCA1-mediated end resection but also has a secondary role in promoting BLM function in DNA repair.
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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.