ArticleNature structural & molecular biology2026
Resolution of R-loops and transcription-replication conflicts by SETX-BRCA1-BARD1 complex.
Article in Nature structural & molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- R-loops in colorectal cancer: mechanisms, mapping strategies, and therapeutic opportunities.Molecular biology reports · 2026Review
- HELZ-BRCA2 complex resolves R-loops to drive transcription-coupled homologous recombination.Nature communications · 2026Article
- G quadruplex DNA facilitates a pervasive path to homologous recombination.bioRxiv : the preprint server for biology · 2026Article
- RNA damage signaling primes transcription-coupled repair.Nature structural & molecular biology · 2026Article
- Resolution of R-loops and transcription-replication conflicts by SETX-BRCA1-BARD1 complex.Nature structural & molecular biology · 2026Article
- Distinct mechanisms of recognition of phosphorylated RNAPII C-terminal domain by BRCT repeats of the BRCA1-BARD1 complex.The Journal of biological chemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
39 authors.
Funding
Abstract
Senataxin (SETX), an RNA-DNA helicase, accumulates at transcription pause sites through the tumor suppressor BRCA1. Here, we provide mechanistic insight into how SETX-BRCA1 resolves transcription-associated R-loops to prevent deleterious outcomes. Specifically, we show that full-length SETX unwinds R-loops with broad specificity and that the complex of BRCA1 and its obligatory partner BARD1 binds R-loops and stimulates R-loop unwinding by SETX. BRCA1-BARD1 alleviates the inhibitory effect of RAD52 on SETX-mediated R-loop unwinding. We also demonstrate that phosphorylation of Ser642 in SETX promotes its interaction with BRCA1 through the tandem BRCT domain of the latter. Accordingly, mutations impacting the catalytic domain or Ser642 in SETX lead to R-loop accumulation, transcription-replication conflicts, replication fork stalling and DNA double-strand breaks in human cells. Thus, our results delineate the molecular basis for functional synergy between SETX and BRCA1-BARD1 in R-loop resolution and the mitigation of transcription-replication conflicts to preserve genome integrity.
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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 Socratic graph.