Evidence map›Paper›PMID 25503194›Full record

ArticleNature communications2014

The CDC13-STN1-TEN1 complex stimulates Pol α activity by promoting RNA priming and primase-to-polymerase switch.

Neal F Lue, Jamie Chan, Woodring E Wright, Jerard Hurwitz

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Telomeres and Cancer.Life (Basel, Switzerland) · 2021
    Review

4 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

4 authors at 2 institutions in 1 country.

Neal F LueW. R. Hearst Microbiology Research Center, Department of Microbiology &Immunology, Weill Medical College of Cornell University, New York, New York 10065, USA.
Jamie ChanW. R. Hearst Microbiology Research Center, Department of Microbiology &Immunology, Weill Medical College of Cornell University, New York, New York 10065, USA.
Woodring E WrightDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Jerard HurwitzMolecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.
Memorial Sloan Kettering Cancer Center · USThe University of Texas Southwestern Medical Center · US

Funding

GENE EXPRESSION IN AGING AND DEVELOPMENTR01AG001228 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 1985 to 2018
$7.6M
Cancer Biology Training GrantT32CA124334 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAY, JERRY WILLIAM · 2007 to 2021
$5.3M
Telomere terminal extension and replication: mechanisms and links to DNA repair - SupplementR01GM107287 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI LUE, NEAL F · 2014 to 2023
$2.9M
Studies with the human Cdc45-Mcm2-7-GINS helicase complexR01GM110083 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI HURWITZ, JERARD · 2014 to 2017
$1.2M
Telomerase function and regulation in a new model systemR01GM069507 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI LUE, NEAL F · 2004 to 2007
$1.2M
GENE EXPRESSION IN AGING AND DEVELOPMENTR37AG001228 · NIA · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI WRIGHT, WOODRING ERIK · 1987 to 1996
–
NCI NIH HHS NIH T32 CA124334NCI NIH HHS T32 CA124334NIA NIH HHS AG01228NIA NIH HHS R01 AG001228NIGMS NIH HHS NIH GM107287NIGMS NIH HHS R01 GM069507NIGMS NIH HHS R01 GM107287NIGMS NIH HHS R01 GM110083
6 · The paper itself

Abstract

Emerging evidence suggests that Cdc13-Stn1-Ten1 (CST), an RPA-like ssDNA-binding complex, may regulate primase-Pol α (PP) activity at telomeres constitutively, and at other genomic locations under conditions of replication stress. Here we examine the mechanisms of PP stimulation by CST using purified complexes derived from Candida glabrata. While CST does not enhance isolated DNA polymerase activity, it substantially augments both primase activity and primase-to-polymerase switching. CST also simultaneously shortens the RNA and lengthens the DNA in the chimeric products. Stn1, the most conserved subunit of CST, is alone capable of PP stimulation. Both the N-terminal OB fold and the C-terminal winged-helix domains of Stn1 can bind to the Pol12 subunit of the PP complex and stimulate PP activity. Our findings provide mechanistic insights on a well-conserved pathway of PP regulation that is critical for genome stability.

Indexed as

Gene Expression Regulation, FungalBinding SitesCandida glabrataCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA, FungalDNA Polymerase IDNA PrimaseDNA, Single-StrandedFungal ProteinsGenome, FungalGenomic InstabilityProtein BindingProtein Structure, SecondaryProtein Structure, TertiaryRNA, FungalCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA, FungalDNA Polymerase IDNA PrimaseDNA, Single-StrandedFungal ProteinsRNA, FungalTelomere-Binding Proteins

Identifiers

PMID25503194
PMCPMC4269169
OpenAlexW2036332022

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.