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Signaling by the cJun NH 2 ‐terminal kinase
Author(s) -
Davis Roger J
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.204.1
Subject(s) - kinase , insulin resistance , pathogenesis , phenotype , microbiology and biotechnology , signal transduction , mechanism (biology) , cancer research , phosphorylation , obesity , biology , endocrinology , chemistry , medicine , gene , biochemistry , philosophy , epistemology
The cJun NH2‐terminal kinase (JNK) signaling pathway is implicated in the pathogenesis of diabetes and cancer. High fat diet‐induced obesity causes activation of JNK in target tissues. JNK‐deficient mice are resistant to the effects of feeding a high fat diet, including protection against insulin resistance and failure of obesity development. We have used tissue‐specific JNK‐deficient mice to probe the mechanism of JNK regulation of insulin resistance and obesity. We show that JNK plays different roles in multiple tissues and that the phenotype of whole body JNK‐deficient mice reflects the interactions between these different JNK‐dependent processes. The molecular mechanisms of JNK function in metabolic disease and cancer will be discussed.