Evidence map›Paper›PMID 27852626›Full record

ArticleThe EMBO journal2017

Negative regulation of type I IFN signaling by phosphorylation of STAT2 on T387.

Yuxin Wang, Jing Nan, Belinda Willard, Xin Wang, Jinbo Yang, George R Stark

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Transcriptional control of interferon-stimulated genes.The Journal of biological chemistry · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. FBXW7-mediated stability regulation of signal transducer and activator of transcription 2 in melanoma formation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Review
  14. Differential Regulation of Type I and Type III Interferon Signaling.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Review
  17. Review
  18. Cyclin-dependent kinase activity is required for type I interferon production.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018
    Review
  20. Article
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

6 authors at 2 institutions in 2 countries.

Yuxin WangKey Laboratory of Marine Drugs, Ministry of Education Ocean University of China, Qingdao, Shandong, China.
Jing NanDepartment of Cancer Biology, Lerner Research Institute The Cleveland Clinic Foundation, Cleveland, OH, USA.
Belinda WillardProteomics and Metabolomics Laboratory, Lerner Research Institute The Cleveland Clinic Foundation, Cleveland, OH, USA.
Xin WangDepartment of Immunology, Lerner Research Institute The Cleveland Clinic Foundation, Cleveland, OH, USA.
Jinbo YangKey Laboratory of Marine Drugs, Ministry of Education Ocean University of China, Qingdao, Shandong, China starkg@ccf.org yangjb@ouc.edu.cn.
George R StarkDepartment of Cancer Biology, Lerner Research Institute The Cleveland Clinic Foundation, Cleveland, OH, USA starkg@ccf.org yangjb@ouc.edu.cn.ORCID 0000-0002-8776-9597
Cleveland Clinic · USOcean University of China · CN

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA, STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
LTQ-Orbitrap Velos instrumentS10RR031537 · NCRR · CLEVELAND CLINIC LERNER COM-CWRU · PI WILLARD, BELINDA BELLE · 2011 to 2011
$600k
NCI NIH HHS P01 CA062220NCRR NIH HHS S10 RR031537
6 · The paper itself

Abstract

The transcription factor ISGF3, comprised of IRF9 and tyrosine-phosphorylated STATs 1 and 2, transmits the signal from the type I interferon receptor to the genome. We have discovered a novel phosphorylation of STAT2 on T387 that negatively regulates this response. In most untreated cell types, the majority of STAT2 is phosphorylated on T387 constitutively. In response to interferon-β, the T387A mutant of STAT2 is much more effective than wild-type STAT2 in mediating the expression of many interferon-stimulated genes, in protecting cells against virus infection, and in inhibiting cell growth. Interferon-β-treated cells expressing wild-type STAT2 contain much less ISGF3 capable of binding to an interferon-stimulated response element than do cells expressing T387A STAT2. T387 lies in a cyclin-dependent kinase (CDK) consensus sequence, and CDK inhibitors decrease T387 phosphorylation. Using CDK inhibitors to reverse the constitutive inhibitory phosphorylation of T387 of U-STAT2 might enhance the efficacy of type I interferons in many different clinical settings.

Indexed as

Protein Processing, Post-TranslationalSignal TransductionCell LineHumansInterferon-betaInterferon-Stimulated Gene Factor 3Models, BiologicalPhosphorylationSTAT2 Transcription FactorInterferon-betaInterferon-Stimulated Gene Factor 3STAT2 Transcription Factornegative regulationSTAT2T387 phosphorylationtype I interferon

Identifiers

PMID27852626
PMCPMC5239994
OpenAlexW2550241285

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.