Enables 1-phosphatidylinositol-3-kinase activity. Involved in several processes, including phosphatidylinositol 3-kinase/protein kinase B signal transduction; positive regulation of Rac protein signal transduction; and sphingosine-1-phosphate receptor signaling pathway. Acts upstream of or within several processes, including cellular response to cAMP; negative regulation of fibroblast apoptotic process; and regulation of calcium ion transmembrane transport. Predicted to be located in cytosol and membrane. Predicted to be part of phosphatidylinositol 3-kinase complex, class IA and phosphatidylinositol 3-kinase complex, class IB. Predicted to be active in cytoplasm and plasma membrane. Is expressed in hemolymphoid system and thymus primordium. Human ortholog(s) of this gene implicated in autistic disorder; primary immunodeficiency disease; and swine influenza. Orthologous to human PIK3CG (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma).
4-nonylphenol promotes the reaction [bisphenol A results in increased expression of PIK3CG mRNA] and bisphenol A promotes the reaction [4-nonylphenol results in increased expression of PIK3CG mRNA]
4-nonylphenol promotes the reaction [bisphenol A results in increased expression of PIK3CG mRNA] and bisphenol A promotes the reaction [4-nonylphenol results in increased expression of PIK3CG mRNA]
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [Isoproterenol results in increased activity of PIK3CG protein] and wortmannin inhibits the reaction [Isoproterenol results in increased activity of PIK3CG protein]
[lead acetate results in increased abundance of Lead] which results in decreased expression of PIK3CG mRNA and [lead acetate results in increased abundance of Lead] which results in decreased expression of PIK3CG protein
[lead acetate results in increased abundance of Lead] which results in decreased expression of PIK3CG mRNA and [lead acetate results in increased abundance of Lead] which results in decreased expression of PIK3CG protein
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [tamibarotene results in increased expression of and results in increased activity of PIK3CG protein] and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [tamibarotene results in increased expression of PIK3CG mRNA]
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [Isoproterenol results in increased activity of PIK3CG protein] and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [TGFB1 protein results in decreased expression of PIK3CG mRNA]
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one inhibits the reaction [tamibarotene results in increased expression of and results in increased activity of PIK3CG protein] more ...
PIK3CG protein affects the reaction [zinc chloride results in increased activity of MAP3K1 protein] and PIK3CG protein affects the reaction [zinc chloride results in increased activity of MAPK8 protein]
Improvement of the resistance against early Mycobacterium tuberculosis-infection in the absence of PI3Kγ enzyme is associated with increase of CD4+IL-17+ cells and neutrophils.
Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients.
Repression of microRNA-21 inhibits retinal vascular endothelial cell growth and angiogenesis via PTEN dependent-PI3K/Akt/VEGF signaling pathway in diabetic retinopathy.
Involvement of phosphoinositide 3-kinase gamma in the neuro-inflammatory response and cognitive impairments induced by beta-amyloid 1-40 peptide in mice.
Frontline Science: Coincidental null mutation of Csf2rα in a colony of PI3Kγ-/- mice causes alveolar macrophage deficiency and fatal respiratory viral infection.
Cardioprotection induced by olprinone, a phosphodiesterase III inhibitor, involves phosphatidylinositol-3-OH kinase-Akt and a mitochondrial permeability transition pore during early reperfusion.
The alarmin cytokine, high mobility group box 1, is produced by viable cardiomyocytes and mediates the lipopolysaccharide-induced myocardial dysfunction via a TLR4/phosphatidylinositol 3-kinase gamma pathway.
Tissue kallikrein reverses insulin resistance and attenuates nephropathy in diabetic rats by activation of phosphatidylinositol 3-kinase/protein kinase B and adenosine 5'-monophosphate-activated protein kinase signaling pathways.