how does PI 3-kinase activate the AKt kinase after activation of RTK?
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The Akt Pathway, or PI3K-Akt Pathway is a signal transduction pathway that promotes survival and growth in response to extracellular signals. Key proteins involved are PI3K (phosphatidylinositol 3-kinase) and Akt (Protein Kinase B). Initial stimulation by one of the growth factors causes activation of a cell surface receptor and phosphorylation of PI3K. Activated PI3K then phosphorylates lipids on the plasma membrane, forming second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP3). Akt, a serine/threonine kinase, is recruited to the membrane by interaction with these phosphoinositide docking sites, so that it can be fully activated. Activated Akt mediates downstream responses, including cell survival, growth, proliferation, cell migration and angiogenesis, by phosphorylating a range of intracellular proteins. The pathway is present in all cells of higher eukaryotes and is highly conserved.
The pathway is highly regulated by multiple mechanisms, often involving cross-talk with other signalling pathways. Problems with PI3K-Akt pathway regulation can lead to increase in signalling activity. This has been linked to a range of diseases such as cancer and type II diabetes. A major antagonist of PI3K activity is PTEN (phosphatase and tensin homolog), a tumour suppressor which is often mutated or lost in cancer cells. Akt phosphorylates as many as 100 different substrates, leading to a wide range of effects on cells.
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Answer:
The Akt Pathway, or PI3K-Akt Pathway is a signal transduction pathway that promotes survival and growth in response to extracellular signals. ... Akt, a serine/threonine kinase, is recruited to the membrane by interaction with these phosphoinositide docking sites, so that it can be fully activated.
Explanation:
The phosphoinositide 3-kinase (PI3K) pathway, a critical signal transduction system linking oncogenes and multiple receptor classes to many essential cellular functions, is perhaps the most commonly activated signaling pathway in human cancer. This pathway thus presents both an opportunity and a challenge for cancer therapy. Even as inhibitors that target PI3K isoforms and other major nodes in the pathway including AKT and mTOR reach clinical trials, major issues remain. Here we highlight recent progress made in our understanding of the PI3K pathway and discuss both the promises and challenges for the therapeutic development of agents targeting the PI3K pathway in cancer.
Since its discovery in the 1980s, the family of lipid kinases termed phosphoinositide 3-kinases (PI3Ks) has been found to play key regulatory roles in many cellular processes including cell survival, proliferation and differentiation1-3. As major effectors downstream of receptor tyrosine kinases (RTKs) and G protein coupled receptors (GPCRs), PI3Ks transduce signals from various growth factors and cytokines into intracellular messages by generating phospholipids, which in turn activate the serine/threonine kinase AKT and other downstream effector pathways (FIG. 1). The tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10) is the most important negative regulator of the PI3K signaling pathway4, 5. Recent human cancer genomic studies have revealed that many components of the PI3K pathway are frequently targeted by germline or somatic mutations in a broad spectrum of human cancers. These findings, and the fact that PI3K and other kinases in the PI3K pathway are highly suited for pharmacologic intervention, make this pathway one of the most attractive targets for therapeutic intervention in cancer6.