ArticlePLoS genetics2018
BLM prevents instability of structure-forming DNA sequences at common fragile sites.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 36 citations in OpenAlex.
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Targeting FANCM by antisense oligonucleotides in ALT-positive cancers.Molecular therapy. Nucleic acids · 2025Article
- Discovery of novel serum peptide biomarkers for cholangiocarcinoma recurrence through MALDI-TOF MS and LC-MS/MS peptidome analysis.Scientific reports · 2025Article
- Fast and accurate quantification of double-strand breaks in microsatellites by digital PCR.Biology methods & protocols · 2025Article
- MutSβ protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures.Nucleic acids research · 2024Article
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forks.Nucleic acids research · 2023Article
- Plasma exosome-derived fragile site-associated tumor suppressor as a powerful prognostic predictor for patients with ovarian cancer.Bosnian journal of basic medical sciences · 2022Article
- Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022Review
- Homologous recombination within repetitive DNA.Current opinion in genetics & development · 2021Review
- Translesion polymerase eta both facilitates DNA replication and promotes increased human genetic variation at common fragile sites.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Uncovering an allosteric mode of action for a selective inhibitor of human Bloom syndrome protein.eLife · 2021Article
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- BLM has Contrary Effects on Repeat-Mediated Deletions, based on the Distance of DNA DSBs to a Repeat and Repeat Divergence.Cell reports · 2020Article
- Common fragile sites: protection and repair.Cell & bioscience · 2020Review
- Break-induced replication plays a prominent role in long-range repeat-mediated deletion.The EMBO journal · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Genome instability often arises at common fragile sites (CFSs) leading to cancer-associated chromosomal rearrangements. However, the underlying mechanisms of how CFS protection is achieved is not well understood. We demonstrate that BLM plays an important role in the maintenance of genome stability of structure-forming AT-rich sequences derived from CFSs (CFS-AT). BLM deficiency leads to increased DSB formation and hyper mitotic recombination at CFS-AT and induces instability of the plasmids containing CFS-AT. We further showed that BLM is required for suppression of CFS breakage upon oncogene expression. Both helicase activity and ATR-mediated phosphorylation of BLM are important for preventing genetic instability at CFS-AT sequences. Furthermore, the role of BLM in protecting CFS-AT is not epistatic to that of FANCM, a translocase that is involved in preserving CFS stability. Loss of BLM helicase activity leads to drastic decrease of cell viability in FANCM deficient cells. We propose that BLM and FANCM utilize different mechanisms to remove DNA secondary structures forming at CFS-AT on replication forks, thereby preventing DSB formation and maintaining CFS stability.
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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.