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So far, three distinct MAPK pathways have been described in mammalian cells: the extracellular signal-regulated kinases (ERKs) pathway, the c-Jun amino terminal kinase (JNK) pathway and the p38 MAPK pathway. In general, the ERKs are activated by mitogenic and proliferative stimuli, whereas the JNKs and p38 MAPKs respond to environmental stress, including ultraviolet light, heat, osmotic shock and inflammatory cytokines. Five homologues/isoforms of p38 MAPK have been identified: p38α, p38β, p38γ, p38δ and p38-2. The p38 MAPKs are activated by phosphorylation at the Thr-Gly-Tyr motif by the upstream kinases including MKK3 and 6. These upstream kinases have preferential effects on different p38 isoforms. Of these, p38α is the best characterized and perhaps the most physiologically relevant kinase involved in inflammatory responses. The p38αMAPK pathway is crucial to inflammatory cytokine production and signaling. Several p38 MAPK inhibitors have been shown to block the production of interleukin-1, tumour-necrosis factor and other cytokines. The inhibition of cytokine production seems to result from combined effects at the level of transcription and translation.
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