Evidence map›Paper›PMID 31266943›Full record

ArticleNature communications2019

A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription.

Ekaterini Platanitis, Duygu Demiroz, Anja Schneller, Katrin Fischer, Christophe Capelle, Markus Hartl, Thomas Gossenreiter, Mathias Müller, Maria Novatchkova, Thomas Decker

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

148 citing papers in PubMed, 223 citations in OpenAlex.

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88 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

10 authors at 3 institutions in 1 country.

Ekaterini PlatanitisMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.ORCID http://orcid.org/0000-0002-3371-2819
Duygu DemirozMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.
Anja SchnellerMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.
Katrin FischerMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.
Christophe CapelleMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.
Markus HartlMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.ORCID http://orcid.org/0000-0002-4970-7336
Thomas GossenreiterMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria.ORCID http://orcid.org/0000-0002-2935-4078
Mathias MüllerInstitute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, 1210, Austria.
Maria NovatchkovaInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, 1030, Austria.
Thomas DeckerMax Perutz Labs (MPL), University of Vienna, Vienna, 1030, Austria. thomas.decker@univie.ac.at.ORCID http://orcid.org/0000-0001-9683-0620
University of Vienna · ATInstitute of Molecular Biotechnology · ATUniversity of Veterinary Medicine Vienna · AT

Funding

Austrian Science Fund FWF P 25186Austrian Science Fund FWF P 30992Austrian Science Fund FWF W 1261
6 · The paper itself

Abstract

Cells maintain the balance between homeostasis and inflammation by adapting and integrating the activity of intracellular signaling cascades, including the JAK-STAT pathway. Our understanding of how a tailored switch from homeostasis to a strong receptor-dependent response is coordinated remains limited. Here, we use an integrated transcriptomic and proteomic approach to analyze transcription-factor binding, gene expression and in vivo proximity-dependent labelling of proteins in living cells under homeostatic and interferon (IFN)-induced conditions. We show that interferons (IFN) switch murine macrophages from resting-state to induced gene expression by alternating subunits of transcription factor ISGF3. Whereas preformed STAT2-IRF9 complexes control basal expression of IFN-induced genes (ISG), both type I IFN and IFN-γ cause promoter binding of a complete ISGF3 complex containing STAT1, STAT2 and IRF9. In contrast to the dogmatic view of ISGF3 formation in the cytoplasm, our results suggest a model wherein the assembly of the ISGF3 complex occurs on DNA.

Indexed as

Gene Expression RegulationAnimalsFemaleHumansInterferonsInterferon-Stimulated Gene Factor 3Interferon-Stimulated Gene Factor 3, gamma SubunitMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticRAW 264.7 CellsSTAT1 Transcription FactorSTAT2 Transcription FactorInterferonsInterferon-Stimulated Gene Factor 3Interferon-Stimulated Gene Factor 3, gamma SubunitIsgf3g protein, mouseSTAT1 Transcription FactorSTAT2 Transcription Factor

Identifiers

PMID31266943
PMCPMC6606597
OpenAlexW2955932976

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.