Evidence map›Paper›PMID 22863775›Full record

ArticleThe EMBO journal2012

Human CST promotes telomere duplex replication and general replication restart after fork stalling.

Jason A Stewart, Feng Wang, Mary F Chaiken, Christopher Kasbek, Paul D Chastain, Woodring E Wright, Carolyn M Price

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

162 citing papers in PubMed, 217 citations in OpenAlex.

  1. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
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  17. HeterozygousGenes & development · 2024
    Article
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102 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 3 institutions in 1 country.

Jason A StewartDepartment of Cancer and Cell Biology, University of Cincinnati, Cincinnati, OH 45267, USA.
Feng Wang
Mary F Chaiken
Christopher Kasbek
Paul D Chastain
Woodring E Wright
Carolyn M Price
University of Cincinnati · USThe University of Texas Southwestern Medical Center · USUniversity of North Carolina at Chapel Hill · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A. Troester · 2001 to 2026
$36.3M
GENE EXPRESSION IN AGING AND DEVELOPMENTR01AG001228 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 1985 to 2018
$7.6M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
TELOMERE STRUCTURE IN EUPLOTES CRASSUSR01GM041803 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI PRICE, CAROLYN M · 1995 to 2017
$4.8M
Sunlight and MelanomagenesisR21ES018918 · NIEHS · WILLIAM CAREY UNIVERSITY · PI CHASTAIN, PAUL D, CORDEIRO-STONE, MARILA · 2010 to 2011
$402k
Roles of CST, a novel telomere associated complex, at the DNA replication forkF32GM097833 · NIGMS · UNIVERSITY OF CINCINNATI · PI STEWART, JASON AARON · 2011 to 2012
$69k
TELOMERE STRUCTURE IN EUPLOTES CRASSUSR29GM041803 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI PRICE, CAROLYN M · 1989 to 1993
–
GENE EXPRESSION IN AGING AND DEVELOPMENTR37AG001228 · NIA · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI WRIGHT, WOODRING ERIK · 1987 to 1996
–
NCI NIH HHS T32 CA117846NCI NIH HHS T32CA117846NIA NIH HHS AG01228NIEHS NIH HHS ES018918NIEHS NIH HHS P30 ES010126NIEHS NIH HHS P30ES010126NIEHS NIH HHS R21 ES018918NIGMS NIH HHS F32 GM097833NIGMS NIH HHS F32GM097833NIGMS NIH HHS GM041803NIGMS NIH HHS R01 GM041803
6 · The paper itself

Abstract

Mammalian CST (CTC1-STN1-TEN1) associates with telomeres and depletion of CTC1 or STN1 causes telomere defects. However, the function of mammalian CST remains poorly understood. We show here that depletion of CST subunits leads to both telomeric and non-telomeric phenotypes associated with DNA replication defects. Stable knockdown of CTC1 or STN1 increases the incidence of anaphase bridges and multi-telomeric signals, indicating genomic and telomeric instability. STN1 knockdown also delays replication through the telomere indicating a role in replication fork passage through this natural barrier. Furthermore, we find that STN1 plays a novel role in genome-wide replication restart after hydroxyurea (HU)-induced replication fork stalling. STN1 depletion leads to reduced EdU incorporation after HU release. However, most forks rapidly resume replication, indicating replisome integrity is largely intact and STN1 depletion has little effect on fork restart. Instead, STN1 depletion leads to a decrease in new origin firing. Our findings suggest that CST rescues stalled replication forks during conditions of replication stress, such as those found at natural replication barriers, likely by facilitating dormant origin firing.

Indexed as

DNA ReplicationCell Line, TumorGene Knockdown TechniquesGenomic InstabilityHumansTelomereTelomere-Binding ProteinsTelomeric Repeat Binding Protein 1Ctc1 protein, humanStn1 protein, humanTelomere-Binding ProteinsTelomeric Repeat Binding Protein 1

Identifiers

PMID22863775
PMCPMC3433780
OpenAlexW1923187882

What OpenQuestion holds

Textmetadata
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.