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AKT3 — CRK

Text-mined interactions from Literome

Nelson et al., J Biol Chem 2001 : These data indicate that suppression of Akt and MAPK in the presence of activated p38 results in cell death and a possible mechanism for the enhanced apoptosis produced by the combination of CI-1033 and gemcitabine in MDA-MB-453 cells
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
Kaplan-Albuquerque et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Expression of myr-Akt selectively inhibited AVP induced activation of c-Jun N-terminal kinase and p38 mitogen activated protein kinases, which we have shown are critical for induction of these genes
Wu et al., Am J Physiol Lung Cell Mol Physiol 2005 : Inhibition of p38 , Src, and EGFR kinases with pharmacological inhibitors markedly reduces Akt phosphorylation induced by Zn2+
Diehl et al., J Surg Res 2007 (Breast Neoplasms...) : We found that, in the absence of EGF, p38MAPK activated AKT is necessary for HER-2 overexpressing cells to survive and to form colonies in soft agar
Gills et al., J Biol Chem 2007 : Although PIAs rapidly activated p38 with similar time and dose dependence as Akt inhibition, p38 activation and Akt inhibition were independent events induced by PIAs
Kozono et al., Biochem Biophys Res Commun 2010 : CP55940 ( CB1/CB2 agonist ) induced phosphorylation of the extracellular regulated kinases (ERK) 1/2, p38 mitogen activated protein kinase ( p38MAPK ), and Akt in HGFs. Wound closure by CP55940 in an in-vitro scratch assay was significantly suppressed by inhibitors of MAP kinase kinase ( MEK ), p38MAPK , and phosphoinositol 3-kinase (PI3-K)
He et al., Sichuan Da Xue Xue Bao Yi Xue Ban 2010 : Compared with the nomoxia control, hypoxia enhanced the proliferation of MRC-5 and the expressions of pro-collal, p-p38 and p-AKT ( P < 0.05 ). Curcumin inhibited the hypoxia induced proliferation of MRC and the expression of pro-collal and p-p38 ( P < 0.05 ), but not the expression of p-AKT ( P > 0.05 )
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Li et al., Retrovirology 2013 : Activation of Erk/Akt suppresses p38 due to CCR5 binding, and allows cell survival