Evidence map›Paper›PMID 34811541›Full record

ArticleNature immunology2021

Disrupting Roquin-1 interaction with Regnase-1 induces autoimmunity and enhances antitumor responses.

Gesine Behrens, Stephanie L Edelmann, Timsse Raj, Nina Kronbeck, Thomas Monecke, Elena Davydova, Elaine H Wong, Lisa Kifinger, Florian Giesert, Martin E Kirmaier and 10 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Nature immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Roquin exhibits opposing effects on RNA stem-loop stability through its two ROQ domain binding sites.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Roquin-1 interaction with Regnase-1 inhibits the progression of rheumatoid arthritis via suppressing FGF2 expression and NF-κB pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

20 authors at 6 institutions in 2 countries.

Gesine Behrens *Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Stephanie L Edelmann *Research Unit Molecular Immune Regulation, Helmholtz Zentrum München, Munich, Germany.
Timsse Raj *Institute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.ORCID http://orcid.org/0000-0002-5065-8092
Nina KronbeckInstitute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Thomas MoneckeInstitute of Pharmaceutical Biotechnology, Ulm University, Ulm, Germany.
Elena DavydovaInstitute of Structural Biology, Helmholtz Zentrum München, Neuherberg, Germany.ORCID http://orcid.org/0000-0002-3087-2163
Elaine H WongInstitute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Lisa KifingerResearch Unit Molecular Immune Regulation, Helmholtz Zentrum München, Munich, Germany.ORCID http://orcid.org/0000-0001-6422-057X
Florian GiesertInstitute of Developmental Genetics, Helmholtz Zentrum München, Neuherberg, Germany.ORCID http://orcid.org/0000-0001-6825-8858
Martin E KirmaierCancer and Immunometabolism Research Group at the Gene Center, Ludwig-Maximilians-Universität in Munich, Munich, Germany.
Christine HohnInstitute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Laura S de JongeResearch Unit Molecular Immune Regulation, Helmholtz Zentrum München, Munich, Germany.
Mariano Gonzalez PisfilCore Facility Bioimaging and Walter-Brendel-Centre of Experimental Medicine at the Biomedical Center, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Mingui FuDepartment of Basic Medical Science, School of Medicine, University of Missouri-Kansas City, Kansas City, MO, USA.ORCID http://orcid.org/0000-0001-6315-8372
Sebastian TheurichCancer and Immunometabolism Research Group at the Gene Center, Ludwig-Maximilians-Universität in Munich, Munich, Germany.
Stefan FeskeDepartment of Pathology, New York University School of Medicine, New York, NY, USA.
Naoto KawakamiInstitute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany.
Wolfgang WurstInstitute of Developmental Genetics, Helmholtz Zentrum München, Neuherberg, Germany.
Dierk NiessingInstitute of Pharmaceutical Biotechnology, Ulm University, Ulm, Germany.
Vigo HeissmeyerInstitute for Immunology, Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians-Universität in Munich, Planegg-Martinsried, Germany. vigo.heissmeyer@med.uni-muenchen.de.ORCID http://orcid.org/0000-0002-2263-8545
Ludwig-Maximilians-Universität München · DEHelmholtz Zentrum München · DEUniversität Ulm · DEGerman Center for Neurodegenerative Diseases · DENew York University · USUniversity of Missouri–Kansas City · US

Funding

Ribonuclease-mediated control of sepsis-induced systemic inflammationR15AI138116 · NIAID · UNIVERSITY OF MISSOURI KANSAS CITY · PI FU, MINGUI · 2019 to 2019
$465k
NIAID NIH HHS R15 AI138116
6 · The paper itself

Abstract

Roquin and Regnase-1 proteins bind and post-transcriptionally regulate proinflammatory target messenger RNAs to maintain immune homeostasis. Either the sanroque mutation in Roquin-1 or loss of Regnase-1 cause systemic lupus erythematosus-like phenotypes. Analyzing mice with T cells that lack expression of Roquin-1, its paralog Roquin-2 and Regnase-1 proteins, we detect overlapping or unique phenotypes by comparing individual and combined inactivation. These comprised spontaneous activation, metabolic reprogramming and persistence of T cells leading to autoimmunity. Here, we define an interaction surface in Roquin-1 for binding to Regnase-1 that included the sanroque residue. Mutations in Roquin-1 impairing this interaction and cooperative regulation of targets induced T follicular helper cells, germinal center B cells and autoantibody formation. These mutations also improved the functionality of tumor-specific T cells by promoting their accumulation in the tumor and reducing expression of exhaustion markers. Our data reveal the physical interaction of Roquin-1 with Regnase-1 as a hub to control self-reactivity and effector functions in immune cell therapies.

Indexed as

AutoimmunityCytotoxicity, ImmunologicImmunotherapy, AdoptiveAnimalsFemaleHEK293 CellsHeLa CellsHumansImmunity, HumoralMaleMelanoma, ExperimentalMiceMice, Inbred C57BLMice, TransgenicMutationPhenotypeRc3h1 protein, mouseRepressor ProteinsRibonucleasesroquin-2 protein, mouseUbiquitin-Protein LigasesZc3h12a protein, mouse

Identifiers

PMID34811541
PMCPMC8996344
OpenAlexW3216810727

What OpenQuestion holds

Textmetadata
LicenceTDM
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.