ArticleMolecular cell2025
RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Poly(ADP-Ribose) polymerase1 Has Potential to Facilitate the Nucleosome Disassembly.International journal of molecular sciences · 2026Article
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- Article
- MDS/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops.Nucleic acids research · 2026Article
- MDC1 counteracts replication fork reversal and mediates chemosensitivity in BRCA1/2-deficient tumors.Oncogene · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Chromatin adaptation and histone remodeling as mechanisms of PARP inhibitor resistance and therapeutic vulnerability.Frontiers in pharmacology · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
BRCA1 mutant cancers are homologous recombination (HR) deficient, and their sensitivity to anti-cancer therapies such as poly (ADP-ribose) polymerase (PARP) inhibitors (PARPi) has long been attributed to this defect. Accordingly, the HR marker, RAD51 foci have been widely used as biomarkers of PARPi response. However, single-stranded DNA (ssDNA) gaps also characterize BRCA1 mutant cells and have been implicated in PARPi sensitivity. Here, unexpectedly, we find that RAD51 is essential and enriched in the chromatin of BRCA1-deficient cells, while additional deletion of 53BP1 alleviates this enrichment and dependency. The same pattern evolves along with PARPi resistance following loss of mediator of DNA damage checkpoint 1 (MDC1) or H2AX. Unlike 53BP1 loss, however, loss of MDC1 and H2AX in BRCA1-deficient cells does not restore RAD51 foci, further uncoupling HR from PARPi resistance. Collectively, we propose a model in which ssDNA gaps in BRCA1-deficient cells necessitate post-replicative RAD51 chromatin engagement for cell fitness, diverting RAD51 from other roles and revealing a targetable vulnerability.
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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.