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AKT1 — MYC

Text-mined interactions from Literome

Bellmann et al., Apoptosis 2006 : Furthermore, c-Myc expression repressed the activation of Akt induced by the toxic agents doxorubicin, cisplatin and H ( 2 ) O ( 2 ), and also by the physiological agonists PDGF and insulin
Spinsanti et al., J Neurochem 2006 : In our hands, activated PI-3-K reduced the stability of c-Myc, because ( i ) the PI-3-K inhibitor, LY294002, prevented the reduction in c-Myc levels induced by MPEP ; and ( ii ) over-expression of AKT promoted c-Myc ubiquitination
Pan et al., Cancer Biol Ther 2007 (Aneuploidy...) : We found that overexpression of gamma-catenin caused : ( 1 ) a reduction in E-cadherin and corresponding increase in vimentin levels concomitant with increased cell mobility and migration ; ( 2 ) enhancement in the levels of phosphorylated Akt and Erk in the presence of EGF and ( 3 ) an increase in PTTG and c-Myc protein levels, which are likely to accelerate chromosomal instability and uncontrolled proliferation, respectively, in the affected cells
Gustafson et al., Oncogene 2010 : Phosphorylation of Myc proteins is controlled in-part by the receptor tyrosine kinase/phosphatidylinositol 3-kinase/Akt/mTOR signaling, with additional contributions from Aurora A kinase
Vangamudi et al., Molecular cancer 2010 (Breast Neoplasms) : Furthermore, this effect was concomitant with induction of phosphorylation of AKT ( ser473 ) and its downstream target phospho ( ser9 ) GSK3ß, and increased Cyclin D1 and C-Myc protein levels
Gutierrez et al., J Exp Med 2011 (Precursor T-Cell Lymphoblastic Leukemia-Lymphoma) : Moreover, MYC suppresses pten mRNA levels, suggesting that Akt pathway activation downstream of MYC promotes tumor progression
Bayley et al., Curr Opin Oncol 2012 (Neoplasms) : A growing appreciation of the role of oncogenes and tumor suppressor genes in the Warburg effect was reflected in reports of the regulation of glutamine metabolism by p53, the role of c-Myc in the high glucose uptake of tumors, and the regulation of ectonucleoside triphosphate diphosphohydrolase 5 ( ENTPD5 ) and ATP consumption by AKT
Guo et al., Biochem Biophys Res Commun 2012 (Colorectal Neoplasms) : Activation of Akt induces expression of c-Myc and cyclin E, which are overexpressed in colorectal cancer and play an important role in colorectal cancer cell proliferation
Imran et al., Eur J Cancer 2012 : These findings exhibit anticarcinogenic potential of TIS21 via downregulation of c-Myc expression during ATRA induced differentiation of HL-60 cells involving activation and deactivation of two major c-Myc regulators, Erk1/2 and Akt , respectively