JNK kinase

Figure 5 Structures of small-molecule inhibitors of nonapoptotic cell death. Inhibitors of (a-e) PARP-1, (f) HSP90, (i, j) mitochondrial respiratory complexes I and (k) complexes 2, (I) phosphatidylcholine-specific phospholipase C, (m) acid sphingomyelinase, (n) NADPH oxidase, (o) JNK kinase, (p-s) necroptosis, (t-w) MPTP, and (g, h) antioxidants, (a) 3-aminobenzamide, (b) benadrostin, (c) Nu1025, 8-hydroxy-2-methylquinazolin-4(3H)-one,...

Increased JNKs activation in response to ischemia and reperfusion is observed in an adult rabbit cardiomyocytes model of simulated ischemia and reoxygenation. Attenuation of JNKs activity by transfection with a dominant negative mutant of the upstream activator of JNKs, JNK kinase-2 or JNK interacting protein-1, JIP-1, reduced cell death.151 Furthermore, ischemia and reperfusion induced JNKs activation was decreased in perfused hearts subjected to ischemic preconditioning or heat stress treatment.152... 

TAK-1 can also activate c-jun N-terminal kinase ( JNK) andp38 both of which are MAP kinases. JNK activates the transcription factor AP-1 and p38 is involved in mRNA stabilisation. This pathway is also capable of activating ERF-7 in dendritic cells in response to TLR-7 and TLR-9 ligands. 

SAPK/JNK pathway. Within the SAPK (stress-activated protein kinase) class, the Jun NT-terminal kinases (JNKs) form a subfamily (SAPK/JNK 1-3). 

FIGURE 8.6 Parallel pathways to transcription and the MAP kinase family. The MAP kinases can be classified into three groups, based on the identity of the intermediate residue in their dual phosphorylation motifs (TEY, TGY, or TPY). This classification also defines three distinct signal-transduction pathways indicated as the ERK, the JNK/SAPK, and the p38/HOG pathway, each having unique protein kinases acting upstream. 

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