Evidence map›Paper›PMID 35831295›Full record

ArticleNature communications2022

The intrinsically disordered protein TgIST from Toxoplasma gondii inhibits STAT1 signaling by blocking cofactor recruitment.

Zhou Huang, Hejun Liu, Jay Nix, Rui Xu, Catherine R Knoverek, Gregory R Bowman, Gaya K Amarasinghe, L David Sibley

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. 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
5.9field-weighted citation impact, top 3% 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, 36 citations in OpenAlex.

  1. Article
  2. Dense granule proteins: key mediators ofFrontiers in medicine · 2026
    Review
  3. The structural influence of the oncogenic driver mutation N642H in the STAT5B SH2 domain.Protein science : a publication of the Protein Society · 2025
    Article
  4. Interferons andFrontiers in immunology · 2025
    Article
  5. Article
  6. International journal of molecular sciences · 2024
    Article
  7. The JAK-STAT pathway: from structural biology to cytokine engineering.Signal transduction and targeted therapy · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Mutual regulations betweenFrontiers in immunology · 2024
    Review
  14. Review
  15. A Combination of Four Nuclear Targeted Effectors ProtectsbioRxiv : the preprint server for biology · 2023
    Article
  16. Article
  17. Review
  18. 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

8 authors at 3 institutions in 1 country.

Zhou HuangDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Hejun LiuDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA.ORCID 0000-0002-2412-7853
Jay NixMolecular Biology Consortium, Advanced Light Source, Lawrence Berkeley National Laboratory, Berkeley, CA, 94720, USA.ORCID 0000-0002-4041-4975
Rui XuDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Catherine R KnoverekDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Gregory R BowmanDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, 63110, USA.ORCID 0000-0002-2083-4892
Gaya K AmarasingheDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA.ORCID 0000-0002-0418-9707
L David SibleyDepartment of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO, 63110, USA. sibley@wustl.edu.ORCID 0000-0001-7110-0285
Washington University in St. Louis · USLawrence Berkeley National Laboratory · USScripps Research Institute · US

Funding

Virology BSL4 CoreP01AI120943 · NIAID · WASHINGTON UNIVERSITY · PI Gaya K. Amarasinghe · 2016 to 2026
$30.2M
User Training and OutreachP30GM124169 · NIGMS · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI PAUL David ADAMS, Gregory L Hura · 2017 to 2026
$28.6M
Molecular Basis of Human ToxoplasmosisR01AI118426 · NIAID · WASHINGTON UNIVERSITY · PI SIBLEY, L. DAVID · 2015 to 2024
$6.0M
NIAID NIH HHS P01 AI120943NIAID NIH HHS R01 AI118426NIGMS NIH HHS P30 GM124169
6 · The paper itself

Abstract

Signal transducer and activator of transcription (STAT) proteins communicate from cell-surface receptors to drive transcription of immune response genes. The parasite Toxoplasma gondii blocks STAT1-mediated gene expression by secreting the intrinsically disordered protein TgIST that traffics to the host nucleus, binds phosphorylated STAT1 dimers, and occupies nascent transcription sites that unexpectedly remain silenced. Here we define a core region within internal repeats of TgIST that is necessary and sufficient to block STAT1-mediated gene expression. Cellular, biochemical, mutational, and structural data demonstrate that the repeat region of TgIST adopts a helical conformation upon binding to STAT1 dimers. The binding interface is defined by a groove formed from two loops in the STAT1 SH2 domains that reorient during dimerization. TgIST binding to this newly exposed site at the STAT1 dimer interface alters its conformation and prevents the recruitment of co-transcriptional activators, thus defining the mechanism of blocked transcription.

Indexed as

Intrinsically Disordered ProteinsToxoplasmaInterferon-gammaPhosphorylationSignal Transductionsrc Homology DomainsSTAT1 Transcription FactorInterferon-gammaIntrinsically Disordered ProteinsSTAT1 Transcription Factor

Identifiers

PMID35831295
PMCPMC9279507
OpenAlexW4285085570

What OpenQuestion holds

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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.