The many paths to p38 mitogen-activated protein kinase activation in the immune system.
Signals emanating from many cell-surface receptors and environmental cues converge on mitogen-activated protein kinases (MAPKs), which in turn phosphorylate and activate various transcription factors and other molecular effectors. Members of the p38 MAPK family, which respond to pro-inflammatory cytokines and cellular stresses, are typically activated by serial phosphorylation and activation of upstream kinases (the MAPK cascade). In this Review, I highlight the recent studies that indicate that p38-subfamily members can also be activated by non-canonical mechanisms, at least one of which seems to have an important role in antigen-receptor-activated T cells. These alternative pathways might have particular relevance for cells that participate in immune and inflammatory responses.
Ashwell
Jonathan D
JD
Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. jda@pop.nci.nih.gov
D000818:Animals; D004789:Enzyme Activation / Q000276:immunology*; D006801:Humans; D007107:Immune System / Q000201:enzymology*; D008213:Lymphocyte Activation / Q000276:immunology; D018448:Models, Immunological; D015398:Signal Transduction / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases / Q000276:immunology / Q000378:metabolism*
D048051:p38 Mitogen-Activated Protein Kinases