ArticleMolecular cell2019
SLX4IP Antagonizes Promiscuous BLM Activity during ALT Maintenance.
Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 89 citations in OpenAlex.
- Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.Biomolecules · 2026Review
- R-loops and D-loops: a delicate balance in genomic stability and instability.Cell communication and signaling : CCS · 2026Review
- Complex structural variations functionally inactivate the telomerase chaperone TCAB1 in osteosarcoma.BMC cancer · 2026Article
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- ESCO2 Interacts with TRF1/2 and Facilitates Telomere Maintenance.International journal of molecular sciences · 2026Article
- Article
- Molecular basis of XPF-ERCC1 targeting to SLX4-dependent DNA repair pathways.Nature communications · 2025Article
- The alternative lengthening of telomeres pathway through a DNA repair lens: mechanism and therapeutic opportunities.NAR cancer · 2025Review
- Conserved and unique features of terminal telomeric sequences in ALT-positive cancer cells.eLife · 2025Article
- Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025Article
- SLX4IP acts in parallel to FANCM to limit BLM-dependent replication stress at ALT telomeres.bioRxiv : the preprint server for biology · 2025Article
- Multiple functions of the ALT favorite helicase, BLM.Cell & bioscience · 2025Review
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- Strategic base modifications refine RNA function and reduce CRISPR-Cas9 off-targets.Nucleic acids research · 2025Article
- The single-stranded DNA-binding factor SUB1/PC4 alleviates replication stress at telomeres and is a vulnerability of ALT cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TGF-β superfamily-induced transcriptional activation pathways establish the RAD52-dependent ALT machinery during malignant transformation of MPNSTs.Scientific reports · 2024Article
- SUMO promotes DNA repair protein collaboration to support alternative telomere lengthening in the absence of PML.Genes & development · 2024Article
- Alternative lengthening of telomeres: mechanism and the pathogenesis of cancer.Journal of clinical pathology · 2024Article
- Genome maintenance meets mechanobiology.Chromosoma · 2024Review
- Alternative lengthening of telomeres (ALT) cells viability is dependent on C-rich telomeric RNAs.Nature communications · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
Cancer cells acquire unlimited proliferative capacity by either re-expressing telomerase or inducing alternative lengthening of telomeres (ALT), which relies on telomere recombination. Here, we show that ALT recombination requires coordinate regulation of the SMX and BTR complexes to ensure the appropriate balance of resolution and dissolution activities at recombining telomeres. Critical to this control is SLX4IP, which accumulates at ALT telomeres and interacts with SLX4, XPF, and BLM. Loss of SLX4IP increases ALT-related phenotypes, which is incompatible with cell growth following concomitant loss of SLX4. Inactivation of BLM is sufficient to rescue telomere aggregation and the synthetic growth defect in this context, suggesting that SLX4IP favors SMX-dependent resolution by antagonizing promiscuous BLM activity during ALT recombination. Finally, we show that SLX4IP is inactivated in a subset of ALT-positive osteosarcomas. Collectively, our findings uncover an SLX4IP-dependent regulatory mechanism critical for telomere maintenance in ALT cancer cells.
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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.