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- Be0c8c9a797c57878086be0c23b13c229 NCIT_P378 "BIOCARTA" @default.
- Be0c8c9a797c57878086be0c23b13c229 type Axiom @default.
- Be0c8c9a797c57878086be0c23b13c229 annotatedProperty NCIT_P325 @default.
- Be0c8c9a797c57878086be0c23b13c229 annotatedSource NCIT_C38981 @default.
- Be0c8c9a797c57878086be0c23b13c229 annotatedTarget "Many cell-surface receptors induce production of second messengers like PIP3, phosphatidylinositol 3,4,5-trisphosphate, that convey signals to the cytoplasm from the cell surface. PIP3 signals activate the kinase PDK1, 3-phosphoinositide-dependent protein kinase-1, which in turn activates the kinase AKT, also known as protein kinase B. Proteins phosphorylated by activated AKT promote cell survival. Phosphorylation of Ikappa-B kinase leads to activation of the transcription factor NF-kB to oppose apoptosis. Bad is a protein in the Bcl-2 gene family that opposes Bcl-2 to induce apoptosis. Phosphorylation of Bad by AKT blocks anti-apoptotic activity to promote cell survival. Similarly, phosphorylation of the protease caspase 9 or forkhead transcription factors by AKT block the induction of apoptosis by these factors. AKT promotes cell survival and opposes apoptosis by a variety of routes. (This definition may be outdated - see the DesignNote.)" @default.