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Signaling by PI3K isoforms in summary: growth factors bind their receptors on cell surface and activate the receptor tyrosine kinase (TK) or the G-protein coupled receptor (GPCR), promoting the recruitment of class I PI3Ks. The phosphorylation of PIP2 into PIP3 stimulates the downstream activation of both AKT-dependent and -independent signaling pathways. PTEN acts as regulator, removing the 3′ phosphate from PIP3 inactivating the signal perpetuated by class I PI3K [9].
