The phosphoinositide 3-kinase pathway.

By Lewis C. Cantley. Science, 2002

5,817 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/bc94ab46bf47a79eb2ebc93891fbca46658ad866

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In Molecular Biology

Citations in the corpus

Plasma membrane phosphoinositide organization by protein electrostatics (2005, background): “In adult mammalian cells, phosphorylation of PIP 2 produces PtdIns(3,4,5)P 3 , which acts as a second messenger by serving as a membrane anchor for several protein”
Molecular mechanisms of drug resistance (2005, background): “Activation of PI3K generates phosphatidylinositol 3,4,5-trisphosphate (PIP3), a lipid second messenger essential for the translocation of Akt to the plasma membrane, where it is phosphorylated and activated by 3-phosphoinositide-dependent kinase1 (PDK-1) [222,223].”
Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. (2006, background): “PI3K activation results in the phosphorylation and activation of the Ser/Thr kinase Akt, leading to the downstream phosphorylation of a number of proteins that affect cell survival, cell cycle regulation, protein synthesis, and cellular metabolism (81, 343, 606).”
The TSC1-2 tumor suppressor controls insulin–PI3K signaling via regulation of IRS proteins (2004, methodology): “The signal transduction mechanisms operating downstream of insulin receptor ligation have highlighted the importance both of the receptor tyrosine kinase substrates (insulin receptor substrates, IRS-1 and IRS-2) and the lipid kinase phosphoinositide 3-OH kinase (PI3K; Saltiel, 2001; Saltiel and Kahn”
Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “family of enzymes and have been linked to a diverse group of cellular functions, particularly cell growth, survival, differentiation, and proliferation (Cantley, 2002).”
Ubiquitination regulates PTEN nuclear import and tumor suppression. (2007, background): “This firmly links PTEN action to the cell’s plasma membrane (Cantley, 2002; Di Cristofano and Pandolfi, 2000).”
Amiloride inhibits macropinocytosis by lowering submembranous pH and preventing Rac1 and Cdc42 signaling (2010, background): “Akt becomes phosphorylated at the membrane by PDK1 and 2, which are themselves PIP3-activated kinases (Cantley, 2002; Song et al., 2005).”
Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “PI3K converts the plasma-membrane lipid phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P 2 ) to phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P 3 ), which activates other signalling constituents at the plasma membran”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, background): “In vitro they are capable to convert PtdIns to PtdIns-3-P, PtdIns4-P to PtdIns(3,4)P2, and PtdIns(4,5)P2 to PtdIns(3,4,5)P3, but the in vivo substrate is PtdIns(4,5)P2 [16,17].”
Protective Actions of H2S in Acute Myocardial Infarction and Heart Failure (2017, neutral): “to protect against cardiac injury via inhibition of PKCε (8), Bad, and caspase-9 (24).”