Unknown

Dataset Information

0

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


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.

SUBMITTER: Marquis M 

PROVIDER: S-EPMC3903551 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

altmetric image

Publications


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)-ind  ...[more]

Similar Datasets

| S-EPMC535098 | biostudies-literature
| S-EPMC6200930 | biostudies-literature
| S-EPMC7192585 | biostudies-literature
| S-EPMC4451135 | biostudies-literature
| S-EPMC5333157 | biostudies-literature
| S-EPMC2696359 | biostudies-literature
| S-EPMC4955959 | biostudies-literature
| S-EPMC3237631 | biostudies-literature
| S-EPMC6034182 | biostudies-literature
| S-EPMC5975789 | biostudies-literature