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Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis.
Akt-mediated phosphorylation of XLF impairs non-homologous end-joining DNA repair.
Akt promotes tumorigenesis in part through modulating genomic instability via phosphorylating XLF.
TRAF2 and OTUD7B govern a ubiquitin-dependent switch that regulates mTORC2 signalling.
AKT methylation by SETDB1 promotes AKT kinase activity and oncogenic functions.
Author Correction: Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis.
PRMT5-mediated arginine methylation activates AKT kinase to govern tumorigenesis.
Genetic fusions favor tumorigenesis through degron loss in oncogenes.