Evidence map›Paper›PMID 24475167›Full record

ArticlePloS one2014

The non-classical MAP kinase ERK3 controls T cell activation.

Miriam Marquis, Salix Boulet, Simon Mathien, Justine Rousseau, Paméla Thébault, Jean-François Daudelin, Julie Rooney, Benjamin Turgeon, Claudine Beauchamp, Sylvain Meloche and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Atypical MAPKs in cancer.The FEBS journal · 2025
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Miriam MarquisMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada ; Department of Microbiology, Infectiology and Immunology, University of Montreal, Quebec, Canada.
Salix BouletMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada.
Simon MathienInstitute of Research in Immunology and Cancer, University of Montreal, Quebec, Canada.
Justine RousseauDepartment of Pharmacology and Molecular Biology, University of Montreal, Quebec, Canada ; Institute of Research in Immunology and Cancer, University of Montreal, Quebec, Canada.
Paméla ThébaultMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada.
Jean-François DaudelinMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada.
Julie RooneyMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada.
Benjamin TurgeonDepartment of Pharmacology and Molecular Biology, University of Montreal, Quebec, Canada ; Institute of Research in Immunology and Cancer, University of Montreal, Quebec, Canada.
Claudine BeauchampMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada.
Sylvain MelocheDepartment of Pharmacology and Molecular Biology, University of Montreal, Quebec, Canada ; Institute of Research in Immunology and Cancer, University of Montreal, Quebec, Canada.
Nathalie LabrecqueMaisonneuve-Rosemont Hospital Research Centre, Montreal, Quebec, Canada ; Department of Microbiology, Infectiology and Immunology, University of Montreal, Quebec, Canada ; Department of Medicine, University of Montreal, Quebec, Canada.
Hôpital Maisonneuve-Rosemont · CAUniversité de Montréal · CAInstitute for Research in Immunology and Cancer · CA

Funding

Canadian Institutes of Health Research MOP-93729
6 · The paper itself

Abstract

The classical mitogen-activated protein kinases (MAPKs) ERK1 and ERK2 are activated upon stimulation of cells with a broad range of extracellular signals (including antigens) allowing cellular responses to occur. ERK3 is an atypical member of the MAPK family with highest homology to ERK1/2. Therefore, we evaluated the role of ERK3 in mature T cell response. Mouse resting T cells do not transcribe ERK3 but its expression is induced in both CD4⁺ and CD8⁺ T cells following T cell receptor (TCR)-induced T cell activation. This induction of ERK3 expression in T lymphocytes requires activation of the classical MAPK ERK1 and ERK2. Moreover, ERK3 protein is phosphorylated and associates with MK5 in activated primary T cells. We show that ERK3-deficient T cells have a decreased proliferation rate and are impaired in cytokine secretion following in vitro stimulation with low dose of anti-CD3 antibodies. Our findings identify the atypical MAPK ERK3 as a new and important regulator of TCR-induced T cell activation.

Indexed as

Animalsbeta-GalactosidaseCell ProliferationCytokinesDNA PrimersFlow CytometryGene Expression RegulationImmunity, CellularImmunoblottingImmunoprecipitationLymphocyte ActivationMiceMitogen-Activated Protein Kinase 6Reverse Transcriptase Polymerase Chain ReactionT-Lymphocytesbeta-GalactosidaseCytokinesDNA PrimersMitogen-Activated Protein Kinase 6

Identifiers

PMID24475167
PMCPMC3903551
OpenAlexW2039322311

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.