ArticleNucleic acids research2012
The BLM helicase contributes to telomere maintenance through processing of late-replicating intermediate structures.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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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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Who cites it
102 citing papers in PubMed.
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- Cellular adaptations impact the biological activity of naphthalene diimide G-quadruplex ligands in ALT-positive osteosarcoma cells.Cell death & disease · 2025Article
- Conserved and unique features of terminal telomeric sequences in ALT-positive cancer cells.eLife · 2025Article
- SLX4IP acts in parallel to FANCM to limit BLM-dependent replication stress at ALT telomeres.bioRxiv : the preprint server for biology · 2025Article
- Condensin II interacts with BLM helicase in S phase to maintain genome stability.Communications biology · 2025Article
- A CPC-shelterin-BTR axis regulates mitotic telomere deprotection.Nature communications · 2025Article
- Multiple functions of the ALT favorite helicase, BLM.Cell & bioscience · 2025Review
- Rapid dynamics allow the low-abundance RTEL1 helicase to promote telomere replication.Nucleic acids research · 2025Article
- RECQ4-MUS81 interaction contributes to telomere maintenance with implications to Rothmund-Thomson syndrome.Nature communications · 2025Article
- TRF2-RAP1 represses RAD51-dependent homology-directed telomere repair by promoting BLM-mediated D-loop unwinding and inhibiting BLM-DNA2-dependent 5'-end resection.Nucleic acids research · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Oxidative guanine base damage plays a dual role in regulating productive ALT-associated homology-directed repair.Cell reports · 2024Article
- Structural evidence for elastic tethers connecting separating chromosomes in crane-fly spermatocytes.Life science alliance · 2023Article
- Article
- Histone demethylase KDM2A is a selective vulnerability of cancers relying on alternative telomere maintenance.Nature communications · 2023Article
- Connections between sister and non-sister telomeres of segregating chromatids maintain euploidy.Current biology : CB · 2023Article
- Recognition and unfolding of human telomeric G-quadruplex by short peptide binding identified from the HRDC domain of BLM helicase.RSC advances · 2022Article
- New twists to the ALTernative endings at telomeres.DNA repair · 2022Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorders caused by loss of function of the RecQ helicases WRN or BLM, respectively. BS and WS are characterized by replication defects, hyperrecombination events and chromosomal aberrations, which are hallmarks of cancer. Inefficient replication of the G-rich telomeric strand contributes to chromosome aberrations in WS cells, demonstrating a link between WRN, telomeres and genomic stability. Herein, we provide evidence that BLM also contributes to chromosome-end maintenance. Telomere defects (TDs) are observed in BLM-deficient cells at an elevated frequency, which is similar to cells lacking a functional WRN helicase. Loss of both helicases exacerbates TDs and chromosome aberrations, indicating that BLM and WRN function independently in telomere maintenance. BLM localization, particularly its recruitment to telomeres, changes in response to replication dysfunction, such as in WRN-deficient cells or after aphidicolin treatment. Exposure to replication challenge causes an increase in decatenated deoxyribonucleic acid (DNA) structures and late-replicating intermediates (LRIs), which are visible as BLM-covered ultra-fine bridges (UFBs) in anaphase. A subset of UFBs originates from telomeric DNA and their frequency correlates with telomere replication defects. We propose that the BLM complex contributes to telomere maintenance through its activity in resolving LRIs.
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Registered trials
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