Evidence map›Paper›PMID 30574148›Full record

ArticleFrontiers in immunology2018

The C-Terminal Transactivation Domain of STAT1 Has a Gene-Specific Role in Transactivation and Cofactor Recruitment.

Matthias Parrini, Katrin Meissl, Mojoyinola Joanna Ola, Therese Lederer, Ana Puga, Sebastian Wienerroither, Pavel Kovarik, Thomas Decker, Mathias Müller, Birgit Strobl

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
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  10. DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

10 authors at 3 institutions in 1 country.

Matthias ParriniDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Katrin MeisslDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Mojoyinola Joanna OlaDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Therese LedererDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Ana PugaDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Sebastian WienerroitherMax F. Perutz Laboratories, University of Vienna, Vienna, Austria.
Pavel KovarikMax F. Perutz Laboratories, University of Vienna, Vienna, Austria.
Thomas DeckerMax F. Perutz Laboratories, University of Vienna, Vienna, Austria.
Mathias MüllerDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
Birgit StroblDepartment of Biomedical Sciences, Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna, Vienna, Austria.
University of Veterinary Medicine Vienna · ATMax Perutz Labs · ATUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT1 has a key role in the regulation of innate and adaptive immunity by inducing transcriptional changes in response to cytokines, such as all types of interferons (IFN). STAT1 exist as two splice isoforms, which differ in regard to the C-terminal transactivation domain (TAD). STAT1β lacks the C-terminal TAD and has been previously reported to be a weaker transcriptional activator than STAT1α, although this was strongly dependent on the target gene. The mechanism of this context-dependent effects remained unclear. By using macrophages from mice that only express STAT1β, we investigated the role of the C-terminal TAD during the distinct steps of transcriptional activation of selected target genes in response to IFNγ. We show that the STAT1 C-terminal TAD is absolutely required for the recruitment of RNA polymerase II (Pol II) and for the establishment of active histone marks at the class II major histocompatibility complex transactivator (

Indexed as

AnimalsCells, CulturedGTP-Binding ProteinsHistone CodeInterferon-Stimulated Gene Factor 3, gamma SubunitMacrophagesMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsPrimary Cell CulturePromoter Regions, GeneticProtein DomainsProtein IsoformsRNA Polymerase IISTAT1 Transcription FactorGbp2 protein, mouseGTP-Binding ProteinsInterferon-Stimulated Gene Factor 3, gamma SubunitIsgf3g protein, mouseMHC class II transactivator proteinNuclear ProteinsProtein IsoformsRNA Polymerase IIStat1 protein, mouseSTAT1 Transcription FactorStat2 protein, mouseSTAT2 Transcription FactorTrans-ActivatorsIFNγinterferon regulatory factor 1 (IRF1)IRF8macrophagemediatorRNA polymerase IIsignal transducer and activator of transcriptiontranscriptional coactivator

Identifiers

PMID30574148
PMCPMC6291510
OpenAlexW2902593728

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.