The PI3K-Akt pathway promotes metabolism, proliferation, cell survival, growth and angiogenesis through phosphorylation of downstream substrates. Key proteins in this pathway are phosphatidylinositol 3-kinase (PI3K) and Akt/Protein Kinase B. Research into this pathway began with the discovery of the oncogene ATK8 in 1977 and the cloning of PKB/Akt in 1991. It was later found that PI3K activates Akt and that phospholipids generated by PI3K are required for Akt activation.

1. pi3k-akt signaling pathway
PI3K-Akt Pathway is an intracellular signal transduction pathway that promotes
metabolism, proliferation, cell survival, growth and angiogenesis in response to
extracellular signals. This is mediated through serine and/or threonine
phosphorylation of a range of downstream substrates. Key proteins involved are
phosphatidylinositol 3-kinase (PI3K) and Akt/Protein Kinase B.
The origins of PKB/Akt research can be traced back to the discovery in 1977, by Staal
and co-workers, which is a previously undescribed oncogene in a virus termed ATK8.
And this cell-derived oncogenic sequence were isolated and named akt. In 1991,
three independent research teams identified genes corresponding to PKB/Akt. These
three cloning papers established PKB/Akt as a novel phospho-protein kinase that was
widely expressed, and paved the way for future experiments into the role of PKB/Akt
in diverse cellular processes. An enzyme termed phosphatidylinositol 3-kinase (PI3K)
had been isolated in 1990 by the group of Cantley. In 1995 Richard Roth and his
colleagues reported that Akt was activated by insulin. Then, several researches
suggested that membrane phospholipids generated by PI3K were an integral element
required for PKB/Akt activation.
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