Signal transduction by tumor necrosis factor mediated by JNK protein kinases.

作者: H K Sluss , T Barrett , B Dérijard , R J Davis

DOI: 10.1128/MCB.14.12.8376

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摘要: Abstract JNK protein kinases are distantly related to mitogen-activated (ERKs) and activated by dual phosphorylation on Tyr Thr. The JNK kinase group includes the 46-kDa isoform JNK1. Here we describe molecular cloning of a second member group, 55-kDa JNK2. activities both isoforms markedly increased exposure cells UV radiation. Furthermore, activation is observed in treated with tumor necrosis factor. Although phosphorylate NH2-terminal domain transcription factor c-Jun, activity JNK2 was approximately 10-fold greater than that This difference c-Jun correlates binding compared distinct vitro biochemical properties these suggest they may have different functions vivo. Evidence favor this hypothesis obtained from observation JNK1, but not JNK2, complements defect expression HOG1 yeast Saccharomyces cerevisiae. Together, data indicate role for signal transduction pathway initiated proinflammatory cytokines

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