Evidence map›Paper›PMID 29162862›Full record

ArticleScientific reports2017

TYK2-induced phosphorylation of Y640 suppresses STAT3 transcriptional activity.

Raffaele Mori, Joris Wauman, Laura Icardi, José Van der Heyden, Lode De Cauwer, Frank Peelman, Karolien De Bosscher, Jan Tavernier

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

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  10. Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022
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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

8 authors at 3 institutions in 2 countries.

Raffaele MoriReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.
Joris WaumanReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.
Laura IcardiReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.ORCID 0000-0002-8936-1691
José Van der HeydenReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.
Lode De CauwerReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.ORCID 0000-0002-6928-8271
Frank PeelmanReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.
Karolien De BosscherReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium.
Jan TavernierReceptor Research Laboratories, Cytokine Receptor Lab, VIB-UGent Center for Medical Biotechnology, 9000, Ghent, Belgium. jan.tavernier@vib-ugent.be.
Ghent University · BEAblynx (Belgium) · BEVita-Salute San Raffaele University · IT

Funding

European Research Council 340941
6 · The paper itself

Abstract

STAT3 is a pleiotropic transcription factor involved in homeostatic and host defense processes in the human body. It is activated by numerous cytokines and growth factors and generates a series of cellular effects. Of the STAT-mediated signal transduction pathways, STAT3 transcriptional control is best understood. Jak kinase dependent activation of STAT3 relies on Y705 phosphorylation triggering a conformational switch that is stabilized by intermolecular interactions between SH2 domains and the pY705 motif. We here show that a second tyrosine phosphorylation within the SH2 domain at position Y640, induced by Tyk2, negatively controls STAT3 activity. The Y640F mutation leads to stabilization of activated STAT3 homodimers, accelerated nuclear translocation and superior transcriptional activity following IL-6 and LIF stimulation. Moreover, it unlocks type I IFN-dependent STAT3 signalling in cells that are normally refractory to STAT3 transcriptional activation.

Indexed as

Transcription, GeneticAnimalsCell NucleusHEK293 CellsHumansInterferon-alphaMiceMutant ProteinsMutationNIH 3T3 CellsPhosphorylationPhosphotyrosinePromoter Regions, GeneticProtein BindingProtein DomainsProtein MultimerizationInterferon-alphaMutant ProteinsPhosphotyrosineSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinTYK2 Kinase

Identifiers

PMID29162862
PMCPMC5698428
OpenAlexW2768664330

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.