ArticlePLoS genetics2015
The Shelterin TIN2 Subunit Mediates Recruitment of Telomerase to Telomeres.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 64 citations in OpenAlex.
- Biogenesis and Regulation of Telomerase during Development and Cancer.Cold Spring Harbor perspectives in biology · 2026Review
- C-Terminal Extended Domain-Independent Telomere Maintenance: Modeling the Function of TIN2 Isoforms inInternational journal of molecular sciences · 2025Article
- Canonical and non-canonical functions of the non-coding RNA component (TERC) of telomerase complex.Cell & bioscience · 2025Review
- A persistent variant telomere sequence in a human pedigree.Nature communications · 2024Article
- Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024Review
- Effects of HSV-G47Δ Oncolytic Virus on Telomerase and Telomere Length Alterations in Glioblastoma Multiforme Cancer Stem Cells Under Hypoxia and Normoxia Conditions.Current cancer drug targets · 2024Article
- Maternal stress-induced changes in adolescent and adult offspring: Neurobehavioural improvement and telomere maintenance.Heliyon · 2023Article
- Orchestrating nucleic acid-protein interactions at chromosome ends: telomerase mechanisms come into focus.Nature structural & molecular biology · 2023Review
- CTC1 OB-B interaction with TPP1 terminates telomerase and prevents telomere overextension.Nucleic acids research · 2023Article
- Genomic Fingerprint Associated with Familial Idiopathic Pulmonary Fibrosis: A Review.International journal of medical sciences · 2023Review
- Editing TINF2 as a potential therapeutic approach to restore telomere length in dyskeratosis congenita.Blood · 2022Article
- TIN2 deficiency leads to ALT-associated phenotypes and differentiation defects in embryonic stem cells.Stem cell reports · 2022Article
- Review
- Differential impact of a dyskeratosis congenita mutation in TPP1 on mouse hematopoiesis and germline.Life science alliance · 2022Article
- Telomeres and Age-Related Diseases.Biomedicines · 2021Review
- TAZ maintains telomere length in TNBC cells by mediating Rad51C expression.Breast cancer research : BCR · 2021Article
- Diverse telomeres in trypanosomatids.Parasitology · 2021Article
- The structurally conserved TELR region on shelterin protein TPP1 is essential for telomerase processivity but not recruitment.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.Frontiers in cell and developmental biology · 2021Review
- Role of Telomeres and Telomeric Proteins in Human Malignancies and Their Therapeutic Potential.Cancers · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Dyskeratosis Congenita (DC) is a heritable multi-system disorder caused by abnormally short telomeres. Clinically diagnosed by the mucocutaneous symptoms, DC patients are at high risk for bone marrow failure, pulmonary fibrosis, and multiple types of cancers. We have recapitulated the most common DC-causing mutation in the shelterin component TIN2 by introducing a TIN2-R282H mutation into cultured telomerase-positive human cells via a knock-in approach. The resulting heterozygous TIN2-R282H mutation does not perturb occupancy of other shelterin components on telomeres, result in activation of telomeric DNA damage signaling or exhibit other characteristics indicative of a telomere deprotection defect. Using a novel assay that monitors the frequency and extension rate of telomerase activity at individual telomeres, we show instead that telomerase elongates telomeres at a reduced frequency in TIN2-R282H heterozygous cells; this recruitment defect is further corroborated by examining the effect of this mutation on telomerase-telomere co-localization. These observations suggest a direct role for TIN2 in mediating telomere length through telomerase, separable from its role in telomere protection.
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What OpenQuestion holds
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.