Evidence map›Paper›PMID 19596237›Full record

ArticleCell2009

Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication.

Agnel Sfeir, Settapong T Kosiyatrakul, Dirk Hockemeyer, Sheila L MacRae, Jan Karlseder, Carl L Schildkraut, Titia de Lange

Open access · greenAbstract read
In one paragraph

Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 657 papers.

0numbers the graph read from it
0cells of the map it votes in
657citing papers in PubMed
31.0field-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

657 citing papers in PubMed, 983 citations in OpenAlex.

  1. Review
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  13. Cancer-associated TRF1 mutations alter PARP1 interaction dynamics: an in silico study.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  14. ESCO2 Interacts with TRF1/2 and Facilitates Telomere Maintenance.International journal of molecular sciences · 2026
    Article
  15. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
    Review
  16. Review
  17. Article
  18. CHAMP1 complex promotes heterochromatin assembly and reduces replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Agnel SfeirLaboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Settapong T Kosiyatrakul
Dirk Hockemeyer
Sheila L MacRae
Jan Karlseder
Carl L Schildkraut
Titia de Lange
Rockefeller University · USAlbert Einstein College of Medicine · US

Funding

MECHANISMS OF TELOMERE INDUCED SENESCENCER01AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 1999 to 2026
$11.9M
Molecular Cytology of Human Telomeres: Telomere proteinR37GM049046 · NIGMS · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 2005 to 2014
$5.0M
TELOMERE LENGTH CONTROL BY TRF1 AND TRF2R01CA076027 · NCI · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 1998 to 2012
$4.3M
NCI NIH HHS R01 CA076027NIA NIH HHS R01 AG016642NIGMS NIH HHS R37 GM049046
6 · The paper itself

Abstract

Telomeres protect chromosome ends through the interaction of telomeric repeats with shelterin, a protein complex that represses DNA damage signaling and DNA repair reactions. The telomeric repeats are maintained by telomerase, which solves the end replication problem. We report that the TTAGGG repeat arrays of mammalian telomeres pose a challenge to the DNA replication machinery, giving rise to replication-dependent defects that resemble those of aphidicolin-induced common fragile sites. Gene deletion experiments showed that efficient duplication of telomeres requires the shelterin component TRF1. Without TRF1, telomeres activate the ATR kinase in S phase and show a fragile-site phenotype in metaphase. Single-molecule analysis of replicating telomeres showed that TRF1 promotes efficient replication of TTAGGG repeats and prevents fork stalling. Two helicases implicated in the removal of G4 DNA structures, BLM and RTEL1, were required to repress the fragile-telomere phenotype. These results identify a second telomere replication problem that is solved by the shelterin component TRF1.

Indexed as

Chromosome Fragile SitesDNA ReplicationAnimalsAphidicolinChromosomes, MammalianHumansMetaphaseMiceTelomereTelomeric Repeat Binding Protein 1AphidicolinTelomeric Repeat Binding Protein 1

Identifiers

PMID19596237
PMCPMC2723738
OpenAlexW2161232591

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.