ArticleMolecular cell2010
A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability.
Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.
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Who cites it
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
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- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Mechanism of structure-specific DNA binding by the FANCM branchpoint translocase.Nucleic acids research · 2024Article
- Quantitative proteomics and phosphoproteomics profiling of meiotic divisions in the fission yeast Schizosaccharomyces pombe.Scientific reports · 2024Article
- Conserved genes regulating human sex differentiation, gametogenesis and fertilization.Journal of translational medicine · 2024Review
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- Transcriptional profiles of pulmonary artery endothelial cells in pulmonary hypertension.Scientific reports · 2023Article
- Implications of ubiquitination and the maintenance of replication fork stability in cancer therapy.Bioscience reports · 2023Review
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- The FANCC-FANCE-FANCF complex is evolutionarily conserved and regulates meiotic recombination.Nucleic acids research · 2023Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- And-1 Coordinates with the FANCM Complex to Regulate Fanconi Anemia Signaling and Cisplatin Resistance.Cancer research · 2022Article
- Biochemical and crystallization analysis of the CENP-SX-DNA complex.Acta crystallographica. Section F, Structural biology communications · 2022Article
90 more citing papers are in PubMed but not listed here.
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28 authors at 8 institutions in 5 countries.
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Abstract
FANCM remodels branched DNA structures and plays essential roles in the cellular response to DNA replication stress. Here, we show that FANCM forms a conserved DNA-remodeling complex with a histone-fold heterodimer, MHF. We find that MHF stimulates DNA binding and replication fork remodeling by FANCM. In the cell, FANCM and MHF are rapidly recruited to forks stalled by DNA interstrand crosslinks, and both are required for cellular resistance to such lesions. In vertebrates, FANCM-MHF associates with the Fanconi anemia (FA) core complex, promotes FANCD2 monoubiquitination in response to DNA damage, and suppresses sister-chromatid exchanges. Yeast orthologs of these proteins function together to resist MMS-induced DNA damage and promote gene conversion at blocked replication forks. Thus, FANCM-MHF is an essential DNA-remodeling complex that protects replication forks from yeast to human.
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