Activation of the PI3K-Akt pathway typically begins with the binding of growth factors like EGF or insulin to their respective receptor tyrosine kinases (RTKs). This triggers the dimerization and autophosphorylation of RTKs, creating docking sites for PI3K. Activated PI3K then converts PIP2 to PIP3, facilitating the recruitment and activation of Akt. This process is tightly regulated to ensure normal cellular function.
