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Fig. 2 | Molecular Cancer

Fig. 2

From: The role of RICTOR downstream of receptor tyrosine kinase in cancers

Fig. 2

Schematic representation of an RTK and the downstream PI3K/AKT pathway. PI3K is activated downstream of RTKs by two mechanisms. First, a phosphorylated tyrosine residue on the receptor serves as a docking site for the p85 regulatory subunit of PI3K recruiting the catalytic subunit of PI3K, p110, to the plasma membrane. Second, activated RAS downstream of the RTK induces the membrane translocation and activation of the p110 subunit of PI3K. Activated PI3K converts PIP2 into PIP3, which is a docking site for PDK1 and AKT. AKT is then phosphorylated on Thr308 by PDK1 and on Ser473 by the mTOR kinase from the mTOR complex 2 (mTORC2). mTORC2 is defined by its scaffold protein RICTOR and promotes the stability and activation of AKT, SGK and PKC. AKT activates downstream signals involved in cell proliferation, differentiation, survival and migration

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