Evidence map›Paper›PMID 38418884›Full record

ArticleNature2024

CST-polymerase α-primase solves a second telomere end-replication problem.

Hiroyuki Takai, Valentina Aria, Pamela Borges, Joseph T P Yeeles, Titia de Lange

Open access · greenAbstract read
In one paragraph

Article in Nature, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
17.3field-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

35 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mitotic kinase regulation of DNA replication forks.bioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Hiroyuki Takai *Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY, USA.ORCID 0009-0002-5029-4003
Valentina Aria *Medical Research Council Laboratory of Molecular Biology, Cambridge, UK.
Pamela BorgesLaboratory for Cell Biology and Genetics, Rockefeller University, New York, NY, USA.ORCID 0000-0002-4491-9874
Joseph T P YeelesMedical Research Council Laboratory of Molecular Biology, Cambridge, UK. jyeeles@mrc-lmb.cam.ac.uk.ORCID 0000-0002-2255-2119
Titia de LangeLaboratory for Cell Biology and Genetics, Rockefeller University, New York, NY, USA. delange@rockefeller.edu.ORCID 0000-0002-9267-367X
Rockefeller University · USMRC Laboratory of Molecular Biology · GB

Funding

MECHANISMS OF TELOMERE INDUCED SENESCENCER01AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 1999 to 2026
$11.9M
Genome instability in cancer: telomeres and DNA repairR35CA210036 · NCI · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 2016 to 2026
$10.8M
The interplay of the CST complex and telomerase at human telomeresR50CA243771 · NCI · ROCKEFELLER UNIVERSITY · PI Hiroyuki Takai · 2019 to 2026
$1.2M
Mechanism of the telomeric proliferation limitR56AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 2019 to 2019
$598k
Medical Research Council MC_UP_1201/12NCI NIH HHS R35 CA210036NCI NIH HHS R50 CA243771NIA NIH HHS R01 AG016642NIA NIH HHS R56 AG016642
6 · The paper itself

Abstract

Telomerase adds G-rich telomeric repeats to the 3' ends of telomeres

Indexed as

DNA Polymerase IDNA PrimaseDNA ReplicationTelomereTelomere-Binding ProteinsHumansTelomeraseCtc1 protein, humanDNA polymerase alpha-primaseDNA Polymerase IDNA PrimaseStn1 protein, humanTelomeraseTelomere-Binding ProteinsTen1 protein, human

Identifiers

PMID38418884
PMCPMC11160940
OpenAlexW4392242510

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.