摘要: The c-Jun N-terminal kinase (JNK) group of mitogen-activated protein kinases (MAP kinases) is activated by exposure cells to environmental stress and the treatment with cytokines. mechanism activation JNK mediated dual phosphorylation within subdomain VIII on motif Thr-Pro-Tyr. This MAP MKK4 MKK7. These serve as signalling molecules that integrate a wide array stimuli into pathway. Studies physiological function have been facilitated molecular genetic analysis in Drosophila creation mice targeted disruption components studies demonstrate pathway regulates AP-1 (activator protein-1) transcriptional activity vivo indicate required for embryonic morphogenesis, regulation cellular proliferation apoptosis, response immunological stimuli.