Jun N-terminal kinase

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. 

Deoxycholic acid has also been demonstrated to activate other pivotal oncogenic pathways in CRC cells in vitro including p-catenin/T-cell factor-mediated transcription, extra-cellular signal-regulated kinase activation downstream of the epidermal growth factor receptor and Jun-N-terminal kinase... 

Okubo, Y., Blakesley, V. A., Stannard, B., Gutkind, S., and LeRoith, D., Insulin-like growth factor 1 inhibits the stress-activated protein kinase—Jun N-terminal kinase. J. Biol. Chem. 273, 25961-25966 (1998). 

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). 

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