PI3K/AKT/mTOR signaling pathway: Difference between revisions
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<StructureSection load='3hhm' size='350' side='right' scene='' caption='PI3K (grey) complex with NISH2 P85α and wortmannin (PDB code [[3hhm]]) '> | <StructureSection load='3hhm' size='350' side='right' scene='' caption='PI3K (grey) complex with NISH2 P85α and wortmannin (PDB code [[3hhm]]) '> | ||
The PI3K/AKT/mTOR pathway is an intracellular signaling pathway important in regulating the cell cycle. Therefore, it is directly related to cellular quiescence, proliferation, cancer, and longevity. [[PI3K]] activation phosphorylates and activates AKT, localizing it in the plasma membrane. Protein kinase B (PKB), also known as Akt, is the collective name of a set of three [[Serine/threonine protein kinase|serine/threonine-specific protein kinases]] that play key roles in multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription, and cell migration. AKT can have a number of downstream effects such as activating CREB, inhibiting p27, localizing FOXO in the cytoplasm, activating PtdIns-3ps, and activating mTOR, which can affect transcription of p70 or 4EBP1. | The PI3K/AKT/mTOR pathway is an intracellular signaling pathway important in regulating the cell cycle. Therefore, it is directly related to cellular quiescence, proliferation, cancer, and longevity. [[PI3K]] activation phosphorylates and activates AKT, localizing it in the plasma membrane. Protein kinase B (PKB), also known as Akt, is the collective name of a set of three [[Serine/threonine protein kinase|serine/threonine-specific protein kinases]] that play key roles in multiple cellular processes such as glucose metabolism, apoptosis, cell proliferation, transcription, and cell migration. AKT can have a number of downstream effects such as activating CREB, inhibiting p27, localizing FOXO in the cytoplasm, activating PtdIns-3ps, and activating [[mTOR]], which can affect transcription of p70 or 4EBP1. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> |