![]() ![]() Ultraviolet light and osmotic stress: activation of the JNK cascade through multiple growth factor and cytokine receptors. Autocrine tumor necrosis factor alpha links endoplasmic reticulum stress to the membrane death receptor pathway through IRE1α-mediated NF-κB activation and down-regulation of TRAF2 expression. Hu P, Han Z, Couvillon AD, Kaufman RJ, Exton JH. JNK signaling: regulation and functions based on complex protein-protein partnerships. Zeke A, Misheva M, Reményi A, Bogoyevitch MA. Discordant activation of stress-activated protein kinases or c-Jun NH2-terminal protein kinases in tissues of heat-stressed mice. Diverse roles of JNK and MKK pathways in the brain. Biochimica Biophys Acta (BBA)-Mol Cell Res. Physiological roles of MKK4 and MKK7: insights from animal models. Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73. Smeal T, Binetruy B, Mercola DA, Birrer M, Karin M. In this review, we summarized and discussed the strategies of JNK binding inhibitors and the role of JNK signaling in the pathogenesis of different solid and hematological malignancies. Some of ATP- competitive and ATP non-competitive inhibitors have been developed and widely used in vitro, but this type of inhibitors lack selectivity and inhibits phosphorylation of all JNK substrates and may lead to cellular toxicity. Studies showed that the two major JNK proteins JNK1 and JNK2 have opposite functions in different types of cancers, which need more specification in the design of JNK inhibitors. Therefore, JNKs represent attractive oncogenic targets for cancer therapy using small molecule kinase inhibitors. It is increasingly clear that the continuous activation of JNKs has a role in cancer development and progression. The JNKs are members of mitogen-activated protein kinases (MAPK) which regulate many physiological processes including inflammatory responses, macrophages, cell proliferation, differentiation, survival, and death. ![]()
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