PIK3CG

Phosphoinositide 3-kinases (PI3Ks) phosphorylate inositol lipids and are involved in the immune response. The protein encoded by this gene is a class I catalytic subunit of PI3K. Like other class I catalytic subunits (p110-alpha p110-beta, and p110-delta), the encoded protein binds a p85 regulatory subunit to form PI3K. This gene is located in a commonly deleted segment of chromosome 7 previously identified in myeloid leukemias. Several transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Jun 2015]

Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma

Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Links G-protein coupled receptor activation to PIP3 production. Involved in immune, inflammatory and allergic responses. Modulates leukocyte chemotaxis to inflammatory sites and in response to chemoattractant agents. May control leukocyte polarization and migration by regulating the spatial accumulation of PIP3 and by regulating the organization of F-actin formation and integrin-based adhesion at the leading edge. Controls motility of dendritic cells. Together with PIK3CD is involved in natural killer (NK) cell development and migration towards the sites of inflammation. Participates in T-lymphocyte migration. Regulates T-lymphocyte proliferation and cytokine production. Together with PIK3CD participates in T-lymphocyte development. Required for B-lymphocyte development and signaling. Together with PIK3CD participates in neutrophil respiratory burst. Together with PIK3CD is involved in neutrophil chemotaxis and extravasation. Together with PIK3CB promotes platelet aggregation and thrombosis. Regulates alpha-IIb/beta-3 integrins (ITGA2B/ ITGB3) adhesive function in platelets downstream of P2Y12 through a lipid kinase activity-independent mechanism. May have also a lipid kinase activity-dependent function in platelet aggregation. Involved in endothelial progenitor cell migration. Negative regulator of cardiac contractility. Modulates cardiac contractility by anchoring protein kinase A (PKA) and PDE3B activation, reducing cAMP levels. Regulates cardiac contractility also by promoting beta-adrenergic receptor internalization by binding to GRK2 and by non-muscle tropomyosin phosphorylation. Also has serine/threonine protein kinase activity: both lipid and protein kinase activities are required for beta-adrenergic receptor endocytosis. May also have a scaffolding role in modulating cardiac contractility. Contributes to cardiac hypertrophy under pathological stress. Through simultaneous binding of PDE3B to RAPGEF3 and PIK3R6 is assembled in a signaling complex in which the PI3K gamma complex is activated by RAPGEF3 and which is involved in angiogenesis.

Adaptive immune responseManual Assertion Based On ExperimentTAS:UniProtKB
AngiogenesisIEA:UniProtKB-KW
Cell migrationManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to cAMPIEA:Ensembl
Dendritic cell chemotaxisManual Assertion Based On ExperimentTAS:UniProtKB
EndocytosisIEA:UniProtKB-KW
G protein-coupled receptor signaling pathwayManual Assertion Based On ExperimentIDA:UniProtKB
Hepatocyte apoptotic processIEA:Ensembl
Immune response1 PublicationIC:ComplexPortal
Inflammatory responseManual Assertion Based On ExperimentTAS:UniProtKB
Innate immune responseManual Assertion Based On ExperimentTAS:UniProtKB
Mast cell degranulationManual Assertion Based On ExperimentTAS:UniProtKB
Natural killer cell chemotaxisManual Assertion Based On ExperimentTAS:UniProtKB
Negative regulation of cardiac muscle contractionManual Assertion Based On ExperimentTAS:UniProtKB
Negative regulation of fibroblast apoptotic processIEA:Ensembl
Negative regulation of triglyceride catabolic processIEA:Ensembl
Neutrophil chemotaxisManual Assertion Based On ExperimentTAS:UniProtKB
Neutrophil extravasationManual Assertion Based On ExperimentTAS:UniProtKB
Phosphatidylinositol 3-kinase signalingManual Assertion Based On ExperimentIDA:UniProtKB
Phosphatidylinositol phosphate biosynthetic processManual Assertion Based On ExperimentIBA:GO_Central
Phosphatidylinositol-3-phosphate biosynthetic processManual Assertion Based On ExperimentIBA:GO_Central
Phosphatidylinositol-mediated signalingManual Assertion Based On ExperimentIBA:GO_Central
PhosphorylationManual Assertion Based On ExperimentIDA:MGI
Platelet aggregationManual Assertion Based On ExperimentTAS:UniProtKB
Positive regulation of acute inflammatory responseIEA:Ensembl
Positive regulation of cytokine productionManual Assertion Based On ExperimentTAS:UniProtKB
Positive regulation of cytosolic calcium ion concentrationIEA:Ensembl
Positive regulation of endothelial cell migrationManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of MAP kinase activityManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of protein kinase B signalingManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of Rac protein signal transductionManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of calcium ion transmembrane transportIEA:Ensembl
Regulation of cell adhesion mediated by integrinManual Assertion Based On ExperimentTAS:UniProtKB
Respiratory burst involved in defense responseManual Assertion Based On ExperimentTAS:UniProtKB
Secretory granule localizationIEA:Ensembl
Sphingosine-1-phosphate receptor signaling pathwayManual Assertion Based On ExperimentIMP:BHF-UCL
T cell activationManual Assertion Based On ExperimentTAS:UniProtKB
T cell chemotaxisManual Assertion Based On ExperimentTAS:UniProtKB
T cell proliferationManual Assertion Based On ExperimentTAS:UniProtKB

Cytoplasm
Cell membrane

Autophosphorylation at Ser-1101 has no effect on the phosphatidylinositol-4,5-bisphosphate 3-kinase activity.