Evidence map›Paper›PMID 30944096›Full record

ArticleThe EMBO journal2019

OTUB1 inhibits CNS autoimmunity by preventing IFN-γ-induced hyperactivation of astrocytes.

Xu Wang, Floriana Mulas, Wenjing Yi, Anna Brunn, Gopala Nishanth, Sissy Just, Ari Waisman, Wolfgang Brück, Martina Deckert, Dirk Schlüter

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 62 citations in OpenAlex.

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  15. Astrocytic TIMP-1 regulates production of Anastellin, an inhibitor of oligodendrocyte differentiation and FTY720 responses.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  19. OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2.Signal transduction and targeted therapy · 2023
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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 4 institutions in 1 country.

Xu WangInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany xu.wang@med.ovgu.de schlueter.dirk@mh-hannover.de.ORCID 0000-0001-8428-9339
Floriana MulasInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Wenjing YiInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Anna BrunnDepartment of Neuropathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Gopala NishanthInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Sissy JustInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany.ORCID 0000-0003-4304-8234
Wolfgang BrückInstitute of Neuropathology, University Medical Center Göttingen, Göttingen, Germany.
Martina DeckertDepartment of Neuropathology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Dirk SchlüterInstitute of Medical Microbiology and Hospital Hygiene, Otto-von-Guericke University Magdeburg, Magdeburg, Germany xu.wang@med.ovgu.de schlueter.dirk@mh-hannover.de.ORCID 0000-0003-1478-3328
Medizinische Hochschule Hannover · DEUniversity of Cologne · DEJohannes Gutenberg University Mainz · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell-intrinsic mechanism governing astrocyte function during MS and EAE Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE Mice with astrocyte-specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1-deficient astrocytes were hyperactivated in response to IFN-γ, a fingerprint cytokine of encephalitogenic T cells, and produced more proinflammatory cytokines and chemokines than control astrocytes. Mechanistically, OTUB1 inhibited IFN-γ-induced Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling by K48 deubiquitination and stabilization of the JAK2 inhibitor suppressor of cytokine signaling 1 (SOCS1). Thus, astrocyte-specific OTUB1 is a critical inhibitor of neuroinflammation in CNS autoimmunity.

Indexed as

AnimalsAnimals, NewbornAstrocytesAutoimmunityCells, CulturedCentral Nervous SystemCysteine EndopeptidasesEncephalomyelitis, Autoimmune, ExperimentalFemaleInterferon-gammaMiceMice, Inbred C57BLMice, KnockoutNeurogenic InflammationNeuroimmunomodulationCysteine EndopeptidasesInterferon-gammaOtub1 protein, mouseastrocyteexperimental autoimmune encephalomyelitismultiple sclerosisneuroinflammationOTUB1ubiquitination

Identifiers

PMID30944096
PMCPMC6517825
OpenAlexW2931431500

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.