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Phosphoinositide-3 kinase /Akt pathway

Manning, B. D., and Cantley, L. C. (2003). United at last The tuberous sclerosis complex gene products connect the phosphoinositide 3-kinase/Akt pathway to mammalian target of rapamycin (mTOR) signaling. Biochem. Soc. Trans. 31, 573-578. [Pg.174]

Manning, B. D., Tee, A. R., Logsdon, M. N., Blenis, J., and Candey, L. C. (2002). Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway. Mol. Cell 10, 151—162. [Pg.174]

Cantley, L.C., and Neel, B., 1999, New insights into tumor suppression PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/Akt pathway. Proc. Natl. Acad. Sci. 96 4240-4245. [Pg.327]

Wu, X., Senechal, K., Neshat, M.S., Whang, YE. and Sawyers, C.L. The PTEN/MMACl tumor suppressor phosphatase functions as a negative regulator of the phosphoinositide 3-kinase/Akt pathway (1998) Proc Natl Acad Sd U S A 95, 15587-91... [Pg.246]

Martelli, A., Nyakern, M., Tabellini, G., Bortul, R., Tazzari, P., Evangelisti, C. and Cocco, L. (2006) Phosphoinositide 3 kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia 20, 911-928. [Pg.197]

Zhao, H., Sapolsky, R. M., and Steinberg, G. K. (2006). Phosphoinositide-3-kinase/Akt survival signal pathways are implicated in neuronal survival after stroke. Mol. Neurobiol. 34, 249—269. [Pg.406]

Seo JH, Ahn Y, Lee SR, Yeol YC, Chung HK. 2005. The major target of the endogenously generated reactive oxygen species in response to insulin stimulation is phosphatase and tensin homolog and not phosphoinositide-3 kinase (PI-3 kinase) in the PI-3 kinase/Akt pathway. Mol Biol Cell 16 348-357. [Pg.227]

Shi-Wen X, Chen Y, Denton CP, Eastwood M, Renzoni EA, Bou-Gharios G, Pearson JD, Dashwood M, du Bois RM, Black CM, Leask A, Abraham DJ. 2004. Endothelin-1 promotes myofibroblast induction through the ETA receptor via a rac/phosphoinositide 3-kinase/Akt-dependent pathway and is essential for the enhanced contractile phenotype of fibrotic fibroblasts. Mol Biol Cell 15 2707-2719. [Pg.227]

Hou L, Klann E. 2004. Activation of the phosphoinositide 3-kinase-akt-mammalian target of rapamycin signaling pathway is required for metabotropic glutamate receptor-dependent long-term depression. J Neurosci 24 6352-6361. [Pg.266]

Control of dendritic arborization by the phosphoinositide-3 -kinase-akt-mammalian target of rapamycin pathway. J Neurosci 25 11300-11312. [Pg.266]

Sekulic, A., Hudson, C. C., Homme, J. L., Yin, P., Ottemess, D. M., Kamitz, L. M., andAbraham, R. T. (2000). A direct linkage between the phosphoinositide 3-kinase-AKT signaling pathway and the mammalian target of rapamycin in mitogen-stimulated and transformed cells. Cancer Res. 60, 3504-3513. [Pg.620]

The phosphoinositide-3 kinase (PI3-K)/Akt pathway is activated as a self-defense mechanism of RGCs against injuries inflicted by intravitreal injection of NMDA (Manabe and Lipton, 2003 Nakazawa et al., 2005), episcleral vein cauterization (Kanamori et al., 2004 Kim and Park, 2005), optic nerve clamping (Nakazawa et al., 2003), and translimbal photocoagulation (Levkovitch-Verbin et al., 2007). [Pg.414]

Collectively, the above-mentioned results indicate that the synthetic cannabinoid ligands abn-cbd and 0-1918 act as a selective agonist and silent antagonist, respectively, of a novel vascular endothelial receptor distinct from CBi and CB2 that mediates mesenteric vasodilation, and is coupled to a phosphoinositide (PI)3-kinase/Akt-dependent pathway through Gi/Go. [Pg.612]


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