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Oncogene Proteins, Fusion
Proto-Oncogene Proteins c-akt
Oncogene Protein v-akt
Proto-Oncogene Proteins p21(ras)
Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis.
Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus.
Akt-mediated phosphorylation of XLF impairs non-homologous end-joining DNA repair.
Akt promotes tumorigenesis in part through modulating genomic instability via phosphorylating XLF.
PtdIns(3,4,5)P3-Dependent Activation of the mTORC2 Kinase Complex.
Inhibition of Rb Phosphorylation Leads to mTORC2-Mediated Activation of Akt.
pVHL suppresses kinase activity of Akt in a proline-hydroxylation-dependent manner.
TRAF2 and OTUD7B govern a ubiquitin-dependent switch that regulates mTORC2 signalling.
The p85 isoform of the kinase S6K1 functions as a secreted oncoprotein to facilitate cell migration and tumor growth.
AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions.
PRMT5-mediated arginine methylation activates AKT kinase to govern tumorigenesis.
Genetic fusions favor tumorigenesis through degron loss in oncogenes.
DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.