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AKT3 — HRAS

Text-mined interactions from Literome

Madrid et al., Mol Cell Biol 2000 : In this study, we show that oncogenic H-Ras requires PI3K and Akt to stimulate the transcriptional activity of NF-kappaB
Sheng et al., J Biol Chem 2001 (Cell Transformation, Neoplastic) : Here we demonstrate that inducible expression of oncogenic Ha-Ras results in activation of PKB/Akt in rat intestinal epithelial cells ( RIE-iHa-Ras ), which was blocked by treatment with inhibitors of PI3K activity
Akagi et al., Mol Cell Biol 2002 : The v-Crk induced activation of AKT was greatly enhanced by the overexpression of H-Ras or its guanine nucleotide exchange factor mSOS, which binds to the v-Crk SH3 domain, whereas a dominant negative mutant of H-Ras almost completely suppressed this activation
Choi et al., Oncogene 2004 : Taken together, these findings explain the opposite effects of Ha-Ras and Ki-Ras on modulation of radiosensitivity, and suggest that differential activation of PI3K/Akt and Rac/p38 MAPK signaling by Ha-Ras and Ki-Ras may account for the opposing response to the ionizing radiation
Carón et al., Mol Cancer Ther 2005 (Carcinoma...) : Activated forms of H-RAS and K-RAS differentially regulate membrane association of PI3K, PDK-1, and AKT and the effect of therapeutic kinase inhibitors on cell survival
Song et al., Int J Mol Med 2013 : Piceatannol attenuated the H-ras induced phosphorylation of Akt in a time- and dose dependent manner, whereas resveratrol, at the same concentrations, did not exert an inhibitory effect
Genot et al., Oncogene 1998 : In contrast, p21ras signals are unable to induce Akt/PKB activity in T cell nor is Ras function required for Akt/PKB activation in response to the TCR