ArticleMolecular cell2021
FANCM regulates repair pathway choice at stalled replication forks.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 68 citations in OpenAlex.
- The BRCA1 coiled-coil domain is dispensable for suppression of tandem duplications and tolerance of FANCM loss.The EMBO journal · 2026Article
- BRIP1, a G-quadruplex DNA helicase, protects against AID-induced genomic instability by limiting R-loop accumulation.Molecular medicine (Cambridge, Mass.) · 2026Article
- RNA splicing in health and disease.Molecular biomedicine · 2026Review
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Differences of clinical features, prognosis and genetic mutations in Chinese patients with malignant melanoma and additional primary tumours.Annals of medicine · 2025Article
- The Converging Roles of Nucleases and Helicases in Genome Maintenance and the Aging Process.Life (Basel, Switzerland) · 2025Review
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Whole exome sequencing identifies FANCM as a susceptibility gene for estrogen-receptor-negative breast cancer in Hispanic/Latina women.Nature communications · 2025Article
- Comprehensive genetic and epigenetic characterization of Lynch-like syndrome patients.International journal of cancer · 2025Article
- Targeting FANCM using the antisense oligonucleotides to treat the ALT-positive cancers.Molecular therapy. Nucleic acids · 2025Article
- The Slx4-Rad1-Rad10 nuclease differentially regulates deletions and duplications induced by a replication fork barrier.PLoS genetics · 2025Article
- Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Locking the gates of immortality: targeting alternative lengthening of telomeres (ALT) pathways.Medical oncology (Northwood, London, England) · 2025Review
- BRCA1 and BRCA2: from cancer susceptibility to synthetic lethality.Genes & development · 2025Review
- Mechanisms of tandem duplication in the cancer genome.DNA repair · 2025Review
- Mechanism of structure-specific DNA binding by the FANCM branchpoint translocase.Nucleic acids research · 2024Article
- Review
- CK2-dependent degradation of CBX3 dictates replication fork stalling and PARP inhibitor sensitivity.Science advances · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Repair pathway "choice" at stalled mammalian replication forks is an important determinant of genome stability; however, the underlying mechanisms are poorly understood. FANCM encodes a multi-domain scaffolding and motor protein that interacts with several distinct repair protein complexes at stalled forks. Here, we use defined mutations engineered within endogenous Fancm in mouse embryonic stem cells to study how Fancm regulates stalled fork repair. We find that distinct FANCM repair functions are enacted by molecularly separable scaffolding domains. These findings define FANCM as a key mediator of repair pathway choice at stalled replication forks and reveal its molecular mechanism. Notably, mutations that inactivate FANCM ATPase function disable all its repair functions and "trap" FANCM at stalled forks. We find that Brca1 hypomorphic mutants are synthetic lethal with Fancm null or Fancm ATPase-defective mutants. The ATPase function of FANCM may therefore represent a promising "druggable" target for therapy of BRCA1-linked cancer.
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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.