Akt1, initially identified as the cellular homolog to the retro-viral oncogene v-Akt, is part of the phosphatidyl 3�?kinase (PI3K)-Akt signaling pathway that is activated by diverse cellular stimuli and regulates critical cellular functions such as cell growth, proliferation, and survival. Following phosphorylation of the second messenger PIP2 by PI3K, Akt1 translocates to the cell membrane where it is activated by phosphoinositide-dependent kinase (PDK) 1 and PDK2. The active Akt1 is then able to phosphorylate and activate its substrates, including those that are important for cell proliferation and survival such as TOR and the Bcl-2 homolog Bad. Negative regulation of the PI3K-Akt signaling pathway is mainly accomplished by the lipid phosphatase activity of PTEN which catalyzes the conversion of PIP3 to PIP2, thereby preventing the activation of Akt1. Inactivation of this gene often results in excessive Akt1 activity, often leading to the formation of malignant tumors.
