ArticleCell discovery2016
Bloom syndrome complex promotes FANCM recruitment to stalled replication forks and facilitates both repair and traverse of DNA interstrand crosslinks.
Article in Cell discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 60 citations in OpenAlex.
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres.Neuro-oncology · 2026Article
- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- Review
- Replication stress responses in human lymphocytes change sex-specifically during aging.Nucleic acids research · 2025Article
- SLX4IP acts in parallel to FANCM to limit BLM-dependent replication stress at ALT telomeres.bioRxiv : the preprint server for biology · 2025Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Critical role of alpha spectrin in DNA repair: the importance of μ-calpain and Fanconi anemia proteins.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Erasing marks: Functions of plant deubiquitylating enzymes in modulating the ubiquitin code.The Plant cell · 2024Review
- SMC5/6 Promotes Replication Fork Stability via Negative Regulation of the COP9 Signalosome.International journal of molecular sciences · 2024Article
- Article
- Characterization and acceleration of genome shuffling and ploidy reduction in synthetic allopolyploids by genome sequencing and editing.Nucleic acids research · 2023Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Dynamic Modelling of DNA Repair Pathway at the Molecular Level: A New Perspective.Frontiers in molecular biosciences · 2022Article
- PFKFB3 Inhibition Sensitizes DNA Crosslinking Chemotherapies by Suppressing Fanconi Anemia Repair.Cancers · 2021Article
- PrimPol-mediated repriming facilitates replication traverse of DNA interstrand crosslinks.The EMBO journal · 2021Article
- FANCM regulates repair pathway choice at stalled replication forks.Molecular cell · 2021Article
- Improved Genome Editing through Inhibition of FANCM and Members of the BTR Dissolvase Complex.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Replication Fork Reversal and Protection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The recruitment of FANCM, a conserved DNA translocase and key component of several DNA repair protein complexes, to replication forks stalled by DNA interstrand crosslinks (ICLs) is a step upstream of the Fanconi anemia (FA) repair and replication traverse pathways of ICLs. However, detection of the FANCM recruitment has been technically challenging so that its mechanism remains exclusive. Here, we successfully observed recruitment of FANCM at stalled forks using a newly developed protocol. We report that the FANCM recruitment depends upon its intrinsic DNA translocase activity, and its DNA-binding partner FAAP24. Moreover, it is dependent on the replication checkpoint kinase, ATR; but is independent of the FA core and FANCD2-FANCI complexes, two essential components of the FA pathway, indicating that the FANCM recruitment occurs downstream of ATR but upstream of the FA pathway. Interestingly, the recruitment of FANCM requires its direct interaction with Bloom syndrome complex composed of BLM helicase, Topoisomerase 3α, RMI1 and RMI2; as well as the helicase activity of BLM. We further show that the FANCM-BLM complex interaction is critical for replication stress-induced FANCM hyperphosphorylation, for normal activation of the FA pathway in response to ICLs, and for efficient traverse of ICLs by the replication machinery. Epistasis studies demonstrate that FANCM and BLM work in the same pathway to promote replication traverse of ICLs. We conclude that FANCM and BLM complex work together at stalled forks to promote both FA repair and replication traverse pathways of ICLs.
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.