Fig. 1: As a major downstream effector of receptor tyrosine kinase (RTK) and G protein-coupled receptors, PI3K activates various downstream effectors by generating phospholipids, transducing signals of various growth factors and cytokines into intracellular information. | Cell Death & Disease

Fig. 1: As a major downstream effector of receptor tyrosine kinase (RTK) and G protein-coupled receptors, PI3K activates various downstream effectors by generating phospholipids, transducing signals of various growth factors and cytokines into intracellular information.

From: PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

Fig. 1

The main lipid substrate of PTEN is PIP 3 and indeed PTEN acts as a negative regulator of PI3K/AKT signaling. Among the upstream signaling networks, Akt inactivate TSC1/2 and activate mTORC1. mTORC2 directly phosphorylates Akt at S473 residue leading to its complete activation. This activation of the PI3K/Akt pathway is opposed by PTEN.

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