Gene interactions and pathways from curated databases and text-mining

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AKT3 — PIK3CG

Pathways - manually collected, often from reviews:

  • KEGG Apoptosis: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, indirect effect)
  • KEGG VEGF signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Osteoclast differentiation: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Focal adhesion: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Jak-STAT signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, phosphorylation)
  • KEGG T cell receptor signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG B cell receptor signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein)
  • KEGG Fc gamma R-mediated phagocytosis: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Neurotrophin signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Cholinergic synapse: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Chagas disease (American trypanosomiasis): PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Measles: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Influenza A: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG ErbB signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Colorectal cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Renal cell carcinoma: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, indirect effect)
  • KEGG Prostate cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Melanoma: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Chronic myeloid leukemia: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Acute myeloid leukemia: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Small cell lung cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Non-small cell lung cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Non-small cell lung cancer: PIK3CA/PIK3CB/PIK3CD/PIK3CG → AKT1/AKT2/AKT3 (protein-protein, compound)
  • KEGG Chemokine signaling pathway: PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5 → AKT1/AKT2/AKT3 (protein-protein, compound)
  • WikiPathways Regulation of toll-like receptor signaling pathway: PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3 → AKT3/AKT1/AKT2 (activation)
  • WikiPathways Toll-like Receptor Signaling Pathway: PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3 → AKT3/AKT1/AKT2 (activation)
  • WikiPathways Chemokine signaling pathway: PIK3CA/PIK3CD/PIK3R1/PIK3R2/PIK3R3/PIK3CG/PIK3R5/PIK3CB → AKT1/AKT2/AKT3 (activation)

Text-mined interactions from Literome

Hehl et al., Biochem J 2001 : Expression of a constitutive active PI3Kgamma ( PI3Kgamma-CAAX ) induced GVBD and increased the levels of phosphorylated Akt/protein kinase B and mitogen activated protein kinase ( MAPK )
Oudit et al., Circulation 2003 (Cardiomegaly...) : The lack of PI3Kgamma attenuated the activation of Akt/protein kinase B and extracellular signal regulated kinase 1/2 signaling pathways in cardiac myocytes in response to isoproterenol
Vecchione et al., J Exp Med 2005 (Hypertension) : Conversely, PI3Kgamma was necessary to activate protein kinase B/Akt , which, in turn, enhanced L-type Ca ( 2+ ) channel mediated extracellular Ca ( 2+ ) entry
Kang et al., Proc Natl Acad Sci U S A 2006 (Cell Transformation, Neoplastic) : The p110delta isoform constitutively activates the Akt signaling pathway ; p110gamma activates Akt only in the presence of serum
Guillermet-Guibert et al., Proc Natl Acad Sci U S A 2008 : In macrophages, both p110beta and p110gamma contributed to Akt activation induced by the GPCR agonist complement 5a, but not by the Tyr kinase ligand colony stimulating factor-1
Canobbio et al., Blood 2009 : However, PI3Kbeta, but not PI3Kgamma , enzymatic activity was absolutely required for Akt phosphorylation, Rap1 activation, and platelet aggregation downstream of the immunoreceptor tyrosine based activation motif ( ITAM ) -bearing receptor glycoprotein VI (GPVI)
Haubner et al., PloS one 2010 (Myocardial Reperfusion Injury) : Mechanistically, PI3Kgamma is required for activation of the Reperfusion Injury Salvage Kinase ( RISK ) pathway ( AKT/ERK1/2 ) and regulates phospholamban phosphorylation in the acute injury response