Evidence map›Paper›PMID 28642132›Full record

ArticleBiochemical and biophysical research communications2017

Unphosphorylated STAT3 regulates the antiproliferative, antiviral, and gene-inducing actions of type I interferons.

Susan R Pfeffer, Meiyun Fan, Ziyun Du, Chuan He Yang, Lawrence M Pfeffer

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. The STAT3-Regulated Autophagy Pathway in Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Interleukin-6 and Interferon-α SignalingFrontiers in immunology · 2018
    Article
  13. Review
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

5 authors at 1 institution in 1 country.

Susan R PfefferDepartment of Pathology and Laboratory Medicine, and Center for Cancer Research, University of Tennessee Health Science Center and Memphis, TN 38163, USA.
Meiyun FanDepartment of Pathology and Laboratory Medicine, and Center for Cancer Research, University of Tennessee Health Science Center and Memphis, TN 38163, USA.
Ziyun DuDepartment of Pathology and Laboratory Medicine, and Center for Cancer Research, University of Tennessee Health Science Center and Memphis, TN 38163, USA.
Chuan He YangDepartment of Pathology and Laboratory Medicine, and Center for Cancer Research, University of Tennessee Health Science Center and Memphis, TN 38163, USA.
Lawrence M PfefferDepartment of Pathology and Laboratory Medicine, and Center for Cancer Research, University of Tennessee Health Science Center and Memphis, TN 38163, USA. Electronic address: lpfeffer@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Strategies to improve the antiglioma action of IFN-?: a role for NF-kB inhibitionR01CA133322 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI DAVIDOFF, ANDREW M, PFEFFER, LAWRENCE MARC · 2009 to 2013
$2.6M
IFNARI SIGNALING THROUGH STAT3, PI 3 KINASER01CA073753 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI PFEFFER, LAWRENCE MARC · 1998 to 2007
$2.4M
NCI NIH HHS R01 CA073753NCI NIH HHS R01 CA133322
6 · The paper itself

Abstract

Type I interferon (IFNα/β) induces antiviral and antiproliferative responses in cells through the induction of IFN-stimulated genes (ISGs). Although the roles of IFN-activated STAT1 and STAT2 in the IFN response are well described, the function of STAT3 is poorly characterized. We investigated the role of STAT3 in the biological response to IFNα/β in mouse embryonic fibroblasts (MEFs) with a germ line deletion of STAT3. These STAT3 knockout (STAT3-KO) MEFs were reconstituted with STAT3 or the F705-STAT3 mutant (unphosphorylated STAT3) where the canonical Y705 tyrosine phosphorylation site was mutated. We show that both STAT3 and unphosphorylated STAT3 expression enhance the sensitivity of MEFs to the antiviral, antiproliferative and gene-inducing actions of IFN. By chromatin immunoprecipitation assays, unphosphorylated STAT3 appears to bind, albeit weakly, to select gene promoters to enhance their expression. These results suggest that unphosphorylated STAT3 plays an important role in the IFN response pathway.

Indexed as

AnimalsAntiviral AgentsCell LineCell ProliferationFibroblastsGene Knockout TechniquesInterferon Type IMicePhosphorylationPromoter Regions, GeneticProtein BindingSTAT3 Transcription FactorTranscriptional ActivationAntiviral AgentsInterferon Type ISTAT3 Transcription FactorAntiproliferativeAntiviralGene expressionInterferonSTAT

Identifiers

PMID28642132
PMCPMC5546317
OpenAlexW2651040510

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.