Kinases c-jun N-terminal

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. 

Recent studies in a model of ischemic stroke suggest that the acute neuro-protective effect of melatonin involves activation of the phosphatidylinositol-3-kinase/Akt pathway, whereas ERK-1/2 and c-Jun N-terminal kinase-1/2, in addition to Akt signaling, appear to be involved in its long-term effects (Kilic et al. 2005). These results indicate that melatonin can interact with multiple cellular pathways to produce its diverse physiological effects. Moreover, MTi and MT2 receptors can interact with divergent signaling pathways, as shown by their ability to... 

Interleukin 1 (IL-1) is produced mainly by activated monocytes-macropha-ges, and its principal action is to stimulate thymocytes. A pleiotropic cytokine, IL-1 induces the expression of a large diversity of cytokines such as IL-6, leukaemia inhibitory factor (LIF), and other proinflammatory molecules (Di-marello 1994). IL-1 and TNF-a carry out as part of their function increasing the expression of NF-/cB and JNK (c-Jun N-terminal kinase). The importance of IL-1 in OCS is demonstrated because the IL-1-receptor-deficient mouse is resistant to ovariectomy (OVX)-induced bone loss (Lorenzo et al. 1998). The importance in pathological bone loss is also illustrated by the fact that treatment with IL-1 receptor antagonist slows down bone erosion for patients affected with rheumatoid arthritis (Kwan et al. 2004). IL-1 increases osteoclast differentiation rather than mature osteoclast activity, and infusion of IL-1 into mice induces hypercalcemia and bone resorption. Finally, IL-1 and TNF-a... 

Wong BR, Rho J, Arron J, Robinson E, Orlinick J, Chao M, Kalachikov S, Cayani E, Bartlett FS, III, Frankel WN, Lee SY, Choi Y (1997) TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells. J Biol Chem 272 25190-25194... 

Benhar, M. et al., Enhanced ROS production in oncogenically transformed cells potentiates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and sensitization to genotoxic stress, Mol. Cell. Biol., 21, 6913, 2001. 

Shifrin, V. I. and Anderson P. Trichothecene mycotoxins trigger a ribotoxic stress response that activates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase and induces apoptosis. J. Biol. Chem. 274, 13985, 1999. 

Wang, W., et al.. Activation of the hematopoietic progenitor kinase-1 (HPKl)-dependent, stress-activated c-Jun N-terminal kinase (JNK) pathway by transforming growth factor beta (TGF-beta)-activated kinase (TAKl), a kinase mediator of TGF beta signal transduction. J Biol Chem, 1997,... 

Huang, C., Wy, M., Ding, M., Bowden, G.T. and Dong, Z., 1997, Direct evidence for an important role of sphingomyelinase in ultraviolet-induced ctivation of c-Jun N-terminal kinase. J. Biol. Chem. 272 21153-21151... 

Pyne, S., Chapman, J., Steele, L. and Pyne, N.J., 1996, Sphingomyehn-derived lipids differentially regulate the extracellular signal-regulated kinase 2 (ERK-2) and c-Jun N-terminal kinase (JNK) signal cascades in airway smooth muscle. Ear. J. Biochem. 237 819-826. 

Troy, C.M., Rabacchi, S.A., Xu, Z., et al. (2001) Beta-amyloid-induced neuronal apoptosis requires c-Jun N-terminal kinase activation. J. Neurochem., 77, 157-164. 

W16. Wong, C. K., Zhang, J. P., Lam, C. W. K., Ho, C. Y, and Hjelm, N. M., Sodium salicylate-induced apoptosis of human peripheral blood eosinophils is independent of the activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase. Int. Arch. Allergy Immunol. 121, 44-52 (2000). 

Schroeter, H. et al., Flavonoids protect neurons from oxidized low-density-lipoprotein-induced apoptosis involving c-Jun N-terminal kinase (INK), c-Jun and caspase-3, Biochem. J., 358, 547, 2001. 

Huang, C., Ma, W. Y.,Ryan, C. A., Dong,Z. (1997). Proteinase inhibitors I and II from potatoes speeifieally bloek UV-indueed activator protein-1 activation through a pathway that is independent of extracellular signal-regulated kinases, c-Jun N-terminal kinases, and P38 kinase. Proc. Natl. Acad. Sci. U. S. A., 94, 11957-11962. 

Bogoyevitch MA, Gillespie-Brown J, Ketterman AJ, Fuller SJ, Ben-Levy R, Ashworth A, Marshall CJ, Sugden PH (1996) Stimulation of the stress-activated mitogen-activated protein kinases and c-jun N-terminal kinases are activated by ischemia/reperfusion. Circ Res 79(2) 162-173... 

A MAP kinase module is composed of three kinases where MAP kinase kinase kinase (MAPKKK) will phosphorylate and induce a MAP kinase kinase (MAPKK), which will then phosphorylate and activate a MAP kinase. MAP kinase phosphory-lates either transcription factors that are nonkinase proteins or other kinases that are called MAP kinase-activating protein kinases (MK). There are four distinct classes of MAP kinases, which include ERKs, C-Jun-N-terminal kinases, p38 isoforms and ERK5. 

C-Jun-N-terminal kinases The JNK/Stress-activated protein kinases (SAPKs) do not respond well to mitogens but are strongly activated by agents that induce cellular stress. These kinases phosphorylate C-Jun transcription factor. The sequence of the tripeptide motif for JNK is Thr-Pro-Tyr. The activators of cytokine and tyrosine kinase receptors transduce signal to the upstream MAPKKKs. These... 

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