| First Author | Salvador JM | Year | 2005 |
| Journal | Nat Immunol | Volume | 6 |
| Issue | 4 | Pages | 390-5 |
| PubMed ID | 15735648 | Mgi Jnum | J:97609 |
| Mgi Id | MGI:3575939 | Doi | 10.1038/ni1177 |
| Citation | Salvador JM, et al. (2005) Alternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinases. Nat Immunol 6(4):390-5 |
| abstractText | Signaling-responsive MAP kinases (MAPKs) are key in mediating immune responses and are activated through the phosphorylation of a Thr-X-Tyr motif by upstream MAPK kinases. Here we show that T cells stimulated through the T cell receptor (TCR) used an alternative mechanism in which p38 was phosphorylated on Tyr323 and subsequently autophosphorylated residues Thr180 and Tyr182. This required the TCR-proximal tyrosine kinase Zap70 but not the adaptor protein LAT, which was required for activation of extracellular signal-regulated protein kinase MAPKs. TCR activation of p38 lacking Tyr323 was diminished, and blocking of p38 activity prevented p38 dual phosphorylation in normal T cells but not in B cells. Thus, phosphorylation of Tyr323 dependent on the tyrosine kinase Lck and mediated by Zap70 serves as an important mechanism for TCR activation of p38 in T cells. |
