ArticleThe EMBO journal2010
FANCM regulates DNA chain elongation and is stabilized by S-phase checkpoint signalling.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
59 citing papers in PubMed, 90 citations in OpenAlex.
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Contribution of p53-dependent and -independent mechanisms to upregulation of p21 in Fanconi anemia.PLoS genetics · 2024Article
- Crucial role of the NSE1 RING domain in Smc5/6 stability and FANCM-independent fork progression.Cellular and molecular life sciences : CMLS · 2024Article
- USP1-dependent nucleolytic expansion of PRIMPOL-generated nascent DNA strand discontinuities during replication stress.Nucleic acids research · 2024Article
- Revisiting the BRCA-pathway through the lens of replication gap suppression: "Gaps determine therapy response in BRCA mutant cancer".DNA repair · 2021Review
- Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency.Molecular cell · 2021Article
- DNA topoisomerases: Advances in understanding of cellular roles and multi-protein complexes via structure-function analysis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Review
- Replication Gaps Underlie BRCA Deficiency and Therapy Response.Cancer research · 2021Article
- Coordinated Cut and Bypass: Replication of Interstrand Crosslink-Containing DNA.Frontiers in cell and developmental biology · 2021Review
- Regulation of the Human Papillomavirus Life Cycle by DNA Damage Repair Pathways and Epigenetic Factors.Viruses · 2020Review
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Review
- Dihydropyrimidinase protects from DNA replication stress caused by cytotoxic metabolites.Nucleic acids research · 2020Article
- Copy Number Amplification of DNA Damage Repair Pathways Potentiates Therapeutic Resistance in Cancer.Theranostics · 2020Article
- Article
- TheGenetics · 2019Article
- The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT).Nature communications · 2019Article
- Unstable genomes promote inflammation.Nature · 2019Article
- The Smc5/6 complex regulates the yeast Mph1 helicase at RNA-DNA hybrid-mediated DNA damage.PLoS genetics · 2017Article
- FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
- Commented on by
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FANCM binds and remodels replication fork structures in vitro. We report that in vivo, FANCM controls DNA chain elongation in an ATPase-dependent manner. In the presence of replication inhibitors that do not damage DNA, FANCM counteracts fork movement, possibly by remodelling fork structures. Conversely, through damaged DNA, FANCM promotes replication and recovers stalled forks. Hence, the impact of FANCM on fork progression depends on the underlying hindrance. We further report that signalling through the checkpoint effector kinase Chk1 prevents FANCM from degradation by the proteasome after exposure to DNA damage. FANCM also acts in a feedback loop to stabilize Chk1. We propose that FANCM is a ringmaster in the response to replication stress by physically altering replication fork structures and by providing a tight link to S-phase checkpoint signalling.
Indexed as
Identifiers
What OpenQuestion holds
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.