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Akt-dependent signaling

Patterson C, Mapera S, Li HH, et al. Comparative effects of paclitaxel and rapamycin on smooth muscle migration and survival, Role of Akt-dependent signaling. Arterioscler Thromb Vase Biol 2006 26(7) 1479-1480. [Pg.312]

Banerjee, S., Saxena, N., Sengupta, K., and Baneijee, S.K., ITAlpha-eshadiol-induced VEGF-A expression in rat pituitary tumor cells is mediated through ER independent but PI3K-Akt dependent signaling pathway, Biochem. Biophys. Res. Commun., 300,209-215,2003. [Pg.151]

Cai H, Li Z, Davis ME, Kanner W, Harrison DG, Dudley SC. Jr 2003. Akt dependent phosphorylation of serine 1179 and mitogen-activated protein kinase kinase/extra-cellular signal-regulated kinase 1/2 cooperatively mediate activation of the endothelial nitric-oxide synthase by hydrogen peroxide. Mol Pharmacol 63 325-331. [Pg.258]

Gonzalez E, McGraw TE. Insulin signaling diverges into Akt-dependent and -independent signals to regulate the recruitment/... [Pg.981]

Smit MJ. Kaposi s Sarcoma-Associated Herpesvirus-Encoded G Protein-Coupled Receptor ORF74 Constitutively Activates p44/p42 MAPK and Akt via G(i) and Phospholipase C-Dependent Signaling Pathways. J Virol 2002 76(4) 1744-52. [Pg.51]

Smit, M. J., Verzijl, D., Casarosa, P., Navis, M., Timmerman, H., Leurs, R. (2002). Kaposi s sarcoma-associated herpesvims-encoded G protein-coupled receptor ORF74 constitutively activates p44/p42 MAPK and Akt via G(i) and phospholipase C-dependent signaling pathways. JoMma/TiVo/o, 76, 1744—1752. [Pg.185]

To determine die effects of die inhibitors in vivo, HEK 293 cells were next transfected with HA-asAktl and treated with serially diluted 3-IB-PPl or PriNZ (Fig. 2c). HA-asAktl hypeiphosphoiylation was induced by 3-IB-PPl and PriNZ in a dose-dependent manner, which strongly suggests that induction of phosphorylation results from specific inhibition of Akt downstream signaling and/or specific binding of the Akt inhibitors to die kinase, and not from off-target kinase inhibitoiy activity, as is clearly possible with A-443654. Tlie fact that two structurally distinct Akt inhibitors induced Akt hypeiphosphoiylation... [Pg.59]

While multiple signaling pathways are implicated in mediating the proliferative effects of CXCL12, only Akt activation, p38 activation, and suppression of cAMP levels have been shown to influence the survival response. Vlahakis et al. (2002) demonstrated that CXCL12 regulates survival in CD4-t T lymphocytes via the balance of pro-survival Akt activation and pro-apoptotic p38 activation. Whether the cellular response to CXCL12 was survival or apoptosis depended on coincident activation of these pathways by other factors. [Pg.261]

PKA and PKC are, however, not the only kinases to regulate TRPVl. The Ca /calmodulin-dependent kinase II (CaMKII) sensitizes TRPVl by phosphorylation [57, 58], as does phophatidylinositol 3-kinase (PI3K) via its downstream target AKT [59]. This latter finding links TRPVl to the ERK (extracellular signal-regulated protein kinase) pathway. The non-receptor tyrosine kinase Src likewise potentiates capsaicin-induced currents [60]. [Pg.150]


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