Evidence map›Paper›PMID 28934486›Full record

ArticleNucleic acids research2017

STN1-POLA2 interaction provides a basis for primase-pol α stimulation by human STN1.

Swapna Ganduri, Neal F Lue

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

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  17. Telomeres and Cancer.Life (Basel, Switzerland) · 2021
    Review
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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

2 authors at 1 institution in 1 country.

Swapna GanduriDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Cornell Medical College, New York, NY 10065, USA.
Neal F LueDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Cornell Medical College, New York, NY 10065, USA.
Cornell University · US

Funding

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
NIGMS NIH HHS R01 GM107287
6 · The paper itself

Abstract

The CST (CTC1-STN1-TEN1) complex mediates critical functions in maintaining telomere DNA and overcoming genome-wide replication stress. A conserved biochemical function of the CST complex is its primase-Pol α (PP) stimulatory activity. In this report, we demonstrate the ability of purified human STN1 alone to promote PP activity in vitro. We show that this regulation is mediated primarily by the N-terminal OB fold of STN1, but does not require the DNA-binding activity of this domain. Rather, we observed a strong correlation between the PP-stimulatory activity of STN1 variants and their abilities to bind POLA2. Remarkably, the main binding target of STN1 in POLA2 is the latter's central OB fold domain. In the substrate-free structure of PP, this domain is positioned so as to block nucleic acid entry to the Pol α active site. Thus the STN1-POLA2 interaction may promote the necessary conformational change for nucleic acid delivery to Pol α and subsequent DNA synthesis. A disease-causing mutation in human STN1 engenders a selective defect in POLA2-binding and PP stimulation, indicating that these activities are critical for the in vivo function of STN1. Our findings have implications for the molecular mechanisms of PP, STN1 and STN1-related molecular pathology.

Indexed as

Binding SitesDNADNA Polymerase IDNA PrimaseHumansPoint MutationProtein DomainsProtein SubunitsTelomere-Binding ProteinsDNADNA polymerase alpha-primaseDNA Polymerase IDNA PrimasePOLA2 protein, humanProtein SubunitsStn1 protein, humanTelomere-Binding Proteins

Identifiers

PMID28934486
PMCPMC5766158
OpenAlexW2735565433

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.