C-Jun NH2-terminal kinases

Murasawa S, Matsubara H, Mori Y, et al. Angiotensin II initiates tyrosine kinase Pyk2-dependent signalings leading to activation of Racl-mediated c-Jun NH2-terminal kinase. J Biol Chem 2000 275(35) 26856-26863. 

Chen CY, Wu Z, Karin M. Stabilization of interleukin-2 mRNA by the c-Jun NH2-terminal kinase pathway. Science 1998 280 1945-1949. 

Recently, PUFAs were shown to inhibit T cell activation by blocking key signal transduction events, specifically the activation of c-Jun NH2-terminal kinase (JNK) and NF-AT [62], Furthermore, the expression of CD25 (but not CD69) as well as the production of IL-2 and IL-13 (but not IFN-y, IL-4 and IL-10) was significantly reduced in PUFA-treated peripheral blood T cells. In a separate study, Li and colleagues reported... 

Welsh, N., 1996, Interleukin-l-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF2 in the insulin-producing cell fine RINm5F. J. Biol. Chem. 271 8307-8312. 

Gajate, C., Santos-Beneit, A., ModoleU, M., and Mohinedo, R, 1998, Involvement of c-Jun NH2-terminal kinase activation and c-Jun in the induction of apoptosis by the ether phosphohpid l-0-octadecyl-2-0-methyl-rac-glycero-3-phosphochohne. Mol Pharmacol, 53 602-612... 

Reproduced with permission from Zhang, J. R, Wong, C. K., and Lam, C. W. K. Role of caspases in dexamethasone-induced apoptosis and activation of c-Jun NH2-terminal kinase and p38 mitogen-activated protein kinase in human eosinophils. Clin. Exp. Immunol. 122,20-27 (2000) and Blackwell Science Ltd. 

An important subgroup of MAP kinases has the transcription factor c-Jun as substrate. These kinases are known as c-Jun NH2 terminal kinases (INK) or, due to their activation by stress signals, as stress activated protein kinases (SAPK). The JNK/SAPK proteins are part of their own protein kinase module that conducts stress signals further at the transcription level, and this signaling pathway is therefore known as the JNK/ SAPK pathway. 

Matsuda T, Ferreri K, Todorov I, Kuroda Y, Smith CV, Kandeel F, Mullen Y. 2005. Silymarin protects pancreatic -cells against cytokine-mediated toxicity Implication of c-Jun NH2-terminal kinase and Janus kinase/signal transducer and activator of... 

Chen YN, Cheng CC, Chen JC, Tsauer W, Hsu SL. 2003a. Norcantharidin-induced apoptosis is via the extracellular signal-regulated kinase and c-Jun-NH2-terminal kinase signaling pathways in human hepatoma HepG2 cells. Br J Pharmacol 140 461-470. 

Huang, C Ma, W.-Y., Li, L. and Dong, Z. (1999b) Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway. Cancer Research, 59(13), 3053-58. 

MacKenna DA, Dolfi F, Vuori K, Ruoslahti E. 1998. Extracellular signal-regulated kinase and c-Jun NH2-terminal kinase activation by mechanical stretch is integrin-dependent and matrix-specific in rat cardiac fibroblasts. J Clin Invest 101 301-10. 

Ohtsu, H., Mifune, M., Frank, G. D., et al. 2005. Signal-crosstalk between Rho/ROCK and c-Jun NH2-terminal kinase mediates migration of vascular smooth muscle cells stimulated by angiotensin II. Arterioscler Thromb Vase Biol 25 1831-1836. 

Dziarski, R., Jin, Y.P., Gupta, D. (1996). Differential activation of extracellular signal-regulated kinase (ERK) 1, ERK2, p38, and c-Jun NH2-terminal kinase mitogen-activated protein kinases by bacterial peptidoglycan. J. Infect. Dis. 174 777-85. 

Kurinna, S.M., Tsao, C.C., Nica, A.F., Jiffar, T., and Ruvolo, P.P. (2004). Ceramide promotes apoptosis in lung cancer-derived A549 cells by a mechanism involving c-Jun NH2-terminal kinase. Cancer Res 64, 7852-6. 

Go YM, Patel RP, Maland MC, Park H, Beckman JS, Darley-Usmar VM, Jo H (1999) Evidence for peroxynitrite as a signaling molecule in flow-dependent activation of c-Jun NH2 terminal kinase. Am J Physiol Heart Circ Physiol 277 H1647-H1653... 

Lizundia R, Chaussepied M, Huerre M, WerUng D, Di Santo JP, Langsley G (2006) c-Jun NH2-terminal kinase/c-Jun signaling promotes survival and metastasis of B lymphocytes transformed by Theileria. Cancer Res 66 6105-6110... 

Muhlenbeck F, Haas E, Schwenzer R, Schubert G, Grell M, Smith C, Scheurich P, Wajant H. TRAIL/Apo2L activates c-Jun NH2-terminal kinase (JNK) via caspase-dependent and caspase-independent pathways. J Biol Chem 1998 273 33091-33098. 

Henderson NC, Pollock KJ, Frew J, Mackinnon AC, Flavell RA, Davis RJ, Sethi T, Simpson KJ (2007) Critical role of c-jun (NH2) terminal kinase in paracetamol- induced acute liver failure. 

Dong et al. (1997) used JB6 mouse epidermal cell line, a system that has extensively been used as an in vitro model for tumor promotion studies, to examine antitumor promotion effects of EGCG and theaflavins at the molecular levels. EGCG and theaflavins inhibited EGF- or TP A- induced cell transformation in a dose-dependent manner. EGCG and theaflavins also inhibited AP-1-dependent transcriptional activity and DNA binding activity. This study further showed that the inhibition of AP-1 activation occurs through the inhibition of a c-Jun NH2-terminal kinase dependent pathway. 

Guan, Z., Buckman, S.Y.,MUler, B.W., Springer, L.D., and Morrison. AE. (1998) Interleukin-ip-Induced Cyclooxyge-nase-2 Expression Requires Activation of Both c-Jun NH2-Terminal Kinase and p38 MAPK Signal Pathways in Rat Renal Mesangial Cells. J. Biol. Chem. 273,28670-28676. 

Fig. 13.2. TNFa receptor-signaling activates of all three members of the mitogen activated protein kinase (MARK) family, including the p44/p42 (also termed extracellular signal-related kinases, ERK-1/2), the c-Jun-NH2-terminal kinases (JNK also termed stress-activated protein kinases, SAPK), and p38 MARK (also termed stress/cytokine-activated kinases). U0126 blocks MARK kinase (MEK) phosphorylation of ERKl/2.

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