C-Jun N-terminal kinases (JNK) are distantly related to mitogen-activated protein kinases (ERKs) and are activated by dual phosphorylation on Tyr and Thr. The JNK protein kinase group consists of three isoforms (JNK1, 2, and 3) and regulates transcription activity of the AP-1 complex, and release and regulation of cytochome c (1). JNK becomes activated in vivo in response to pro-inflammatory cytokines or cellular stresses. Its full activation requires the phosphorylation of a threonine and a tyrosine residue in a Thr-Pro-Tyr motif, which can be catalysed by the protein kinases mitogen-activated protein kinase kinase MKK4 and MKK7 (2). Unlike other JNK isoforms, JNK3 is only expressed in the heart and nervous system. JNK3 has been implicated in stress-induced neuronal apoptosis (3).
MAPK signaling pathway
Toll-like receptor signaling pathway
Wnt Signaling Pathway
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