Evidence map›Paper›PMID 22863003›Full record

ArticleCell2012

TPP1 OB-fold domain controls telomere maintenance by recruiting telomerase to chromosome ends.

Franklin L Zhong, Luis F Z Batista, Adam Freund, Matthew F Pech, Andrew S Venteicher, Steven E Artandi

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed
16.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

198 citing papers in PubMed, 307 citations in OpenAlex.

  1. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
  2. Biogenesis and Regulation of Telomerase during Development and Cancer.Cold Spring Harbor perspectives in biology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. A degenerate telomerase RNA directs telomeric DNA synthesis in lepidopteran insects.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
  12. Telomere Reprogramming and Cellular Metabolism: Is There a Link?International journal of molecular sciences · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Telomere maintenance and the DNA damage response: a paradoxical alliance.Frontiers in cell and developmental biology · 2024
    Article
  18. Review
  19. POT1 recruits and regulates CST-Polα/Primase at human telomeres.bioRxiv : the preprint server for biology · 2023
    Article
  20. Review

138 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Franklin L ZhongDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Luis F Z Batista
Adam Freund
Matthew F Pech
Andrew S Venteicher
Steven E Artandi
Stanford University · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Telomeres, Telomerase and Tumor ProgressionR01CA111691 · NCI · STANFORD UNIVERSITY · PI ARTANDI, STEVEN E · 2005 to 2015
$2.8M
Regulation of the Telomerase Protein Component In CancerR01CA125453 · NCI · STANFORD UNIVERSITY · PI ARTANDI, STEVEN E · 2006 to 2015
$2.2M
Defining the telomerase holoenzyme in progenitor cells with agingR01AG033747 · NIA · STANFORD UNIVERSITY · PI ARTANDI, STEVEN E · 2010 to 2014
$1.6M
Defining the telomerase holoenzyme in progenitor cells with agingR56AG033747 · NIA · STANFORD UNIVERSITY · PI ARTANDI, STEVEN E · 2016 to 2016
$597k
NCI NIH HHS 5T32 CA09302NCI NIH HHS CA111691NCI NIH HHS CA125453NCI NIH HHS R01 CA111691NCI NIH HHS R01 CA125453NCI NIH HHS T32 CA009302NIA NIH HHS AG033747NIA NIH HHS R01 AG033747NIA NIH HHS R56 AG033747
6 · The paper itself

Abstract

Telomere synthesis in cancer cells and stem cells involves trafficking of telomerase to Cajal bodies, and telomerase is thought to be recruited to telomeres through interactions with telomere-binding proteins. Here, we show that the OB-fold domain of the telomere-binding protein TPP1 recruits telomerase to telomeres through an association with the telomerase reverse transcriptase TERT. When tethered away from telomeres and other telomere-binding proteins, the TPP1 OB-fold domain is sufficient to recruit telomerase to a heterologous chromatin locus. Expression of a minimal TPP1 OB-fold inhibits telomere maintenance by blocking access of telomerase to its cognate binding site at telomeres. We identify amino acids required for the TPP1-telomerase interaction, including specific loop residues within the TPP1 OB-fold domain and individual residues within TERT, some of which are mutated in a subset of pulmonary fibrosis patients. These data define a potential interface for telomerase-TPP1 interaction required for telomere maintenance and implicate defective telomerase recruitment in telomerase-related disease.

Indexed as

Amino Acid SequenceCell LineCell Line, TumorCoiled BodiesHumansIdiopathic Pulmonary FibrosisModels, MolecularMolecular Sequence DataMutationProtein Structure, TertiarySaccharomyces cerevisiaeSequence AlignmentShelterin ComplexTelomeraseTelomereTelomere-Binding ProteinsACD protein, humanShelterin ComplexTelomeraseTelomere-Binding ProteinsTERT protein, human

Identifiers

PMID22863003
PMCPMC3516183
OpenAlexW2092226916

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.