ArticleNature communications2017
Structural insights into POT1-TPP1 interaction and POT1 C-terminal mutations in human cancer.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 99 citations in OpenAlex.
- How telomere attrition protects against cancer.Nature reviews. Genetics · 2026Review
- Telomere length of both parents contributes to heritable POT1 cancer-predisposition syndrome.Nature communications · 2026Article
- Noncanonical chromosomal-end-specific telomeric repeat arrays in naturally telomerase-negative yeasts.Nucleic acids research · 2026Article
- Telomere length of both parents contribute to heritable POT1 cancer-predisposition syndrome.bioRxiv : the preprint server for biology · 2026Article
- A telomere-based prognostic model incorporating E2F1, MYCN, VPS72, CFAP53, OR8A1, and TXNRD1 for hepatocellular carcinoma.European journal of medical research · 2026Article
- Control of telomerase recruitment and end protection by independent shelterin components.Nature communications · 2026Article
- Active telomere elongation by a subclass of cancer-associated POT1 mutations.Genes & development · 2025Article
- Article
- Phase separation of hnRNPA1 and TERRA regulates telomeric stability.Journal of molecular cell biology · 2025Article
- Combatting cellular immortality in cancers by targeting the shelterin protein complex.Biology direct · 2024Article
- Structural biology of shelterin and telomeric chromatin: the pieces and an unfinished puzzle.Biochemical Society transactions · 2024Review
- Article
- TERT-independent telomere elongation and shelterin dysregulation after pulmonary exposure to stainless-steel welding fume in-vivo.Environmental research · 2024Article
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- The Altered Functions of Shelterin Components in ALT Cells.International journal of molecular sciences · 2023Review
- POT1 recruits and regulates CST-Polα/Primase at human telomeres.bioRxiv : the preprint server for biology · 2023Article
- Article
- Telomerase structural biology comes of age.Current opinion in structural biology · 2022Review
- Comparative genomics of mortal and immortal cnidarians unveils novel keys behind rejuvenation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- DNA Holliday Junction: History, Regulation and Bioactivity.International journal of molecular sciences · 2022Review
5 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
20 authors at 4 institutions in 2 countries.
Funding
Abstract
Mammalian shelterin proteins POT1 and TPP1 form a stable heterodimer that protects chromosome ends and regulates telomerase-mediated telomere extension. However, how POT1 interacts with TPP1 remains unknown. Here we present the crystal structure of the C-terminal portion of human POT1 (POT1C) complexed with the POT1-binding motif of TPP1. The structure shows that POT1C contains two domains, a third OB fold and a Holliday junction resolvase-like domain. Both domains are essential for binding to TPP1. Notably, unlike the heart-shaped structure of ciliated protozoan Oxytricha nova TEBPα-β complex, POT1-TPP1 adopts an elongated V-shaped conformation. In addition, we identify several missense mutations in human cancers that disrupt the POT1C-TPP1 interaction, resulting in POT1 instability. POT1C mutants that bind TPP1 localize to telomeres but fail to repress a DNA damage response and inappropriate repair by A-NHEJ. Our results reveal that POT1 C terminus is essential to prevent initiation of genome instability permissive for tumorigenesis.
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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.