ArticleCell2024
POT1 recruits and regulates CST-Polα/primase at human telomeres.
Article in Cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Peripheral blood telomerase activity and telomerase reverse transcriptase gene expression in psychiatric disorders: a systematic review and meta-analysis.European psychiatry : the journal of the Association of European Psychiatrists · 2025Pooled it
- An updated view on lagging strand DNA replication: implications for the replication stress response.Cell cycle (Georgetown, Tex.) · 2026Article
- Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.Biomolecules · 2026Review
- How telomere attrition protects against cancer.Nature reviews. Genetics · 2026Review
- Fission yeast RPA-TERT-Tpz1TPP1 complex promotes telomere extension and suppresses telomere recombination.PLoS genetics · 2026Article
- Inhibition of lagging strand replication by G-rich telomeric DNA and the shelterin subunit POT1.The EMBO journal · 2026Article
- Fission yeast RPA-TERT-Tpz1bioRxiv : the preprint server for biology · 2026Article
- Conditional deletion of human STN1 leads to telomere dysfunction, genome instability and proliferation defects.Journal of cell science · 2026Article
- Control of telomerase recruitment and end protection by independent shelterin components.Nature communications · 2026Article
- Targeting Telomere Shelterin Protein TPP1 with Elbasvir: Induction of Autophagy and Suppression of Esophageal Cancer Tumorigenesis.Anti-cancer agents in medicinal chemistry · 2026Article
- Whole exome sequencing identified two novel mutations ofFrontiers in cell and developmental biology · 2026Article
- Article
- TERT links telomere length to cancer risk by integrating genomic instability and immune modulation.Discover oncology · 2025Article
- Nanobioreactor detection of space-associated hematopoietic stem and progenitor cell aging.Cell stem cell · 2025Article
- Using the safety scissors: DNA resection regulation at DNA double-strand breaks and telomeres.DNA repair · 2025Review
- TheCells · 2025Article
- Identification of biallelic POLA2 variants in two families with an autosomal recessive telomere biology disorder.European journal of human genetics : EJHG · 2025Article
- Telomere function and regulation from mouse models to human ageing and disease.Nature reviews. Molecular cell biology · 2025Review
- Active telomere elongation by a subclass of cancer-associated POT1 mutations.Genes & development · 2025Article
- The truncated isoform of the receptor for hyaluronan-mediated motility (RHAMMFrontiers in aging · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Telomere maintenance requires the extension of the G-rich telomeric repeat strand by telomerase and the fill-in synthesis of the C-rich strand by Polα/primase. At telomeres, Polα/primase is bound to Ctc1/Stn1/Ten1 (CST), a single-stranded DNA-binding complex. Like mutations in telomerase, mutations affecting CST-Polα/primase result in pathological telomere shortening and cause a telomere biology disorder, Coats plus (CP). We determined cryogenic electron microscopy structures of human CST bound to the shelterin heterodimer POT1/TPP1 that reveal how CST is recruited to telomeres by POT1. Our findings suggest that POT1 hinge phosphorylation is required for CST recruitment, and the complex is formed through conserved interactions involving several residues mutated in CP. Our structural and biochemical data suggest that phosphorylated POT1 holds CST-Polα/primase in an inactive, autoinhibited state until telomerase has extended the telomere ends. We propose that dephosphorylation of POT1 releases CST-Polα/primase into an active state that completes telomere replication through fill-in synthesis.
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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 Socratic graph.