| First Author | Marquis M | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 1 | Pages | e86681 |
| PubMed ID | 24475167 | Mgi Jnum | J:212713 |
| Mgi Id | MGI:5582013 | Doi | 10.1371/journal.pone.0086681 |
| Citation | Marquis M, et al. (2014) The non-classical MAP kinase ERK3 controls T cell activation. PLoS One 9(1):e86681 |
| abstractText | 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. |
