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Human PIK3CG Protein expressed in HEK-293 Cells - ABIN2728968
Hashimoto, Tanaka, Takeda, Ito, Nagano et al.: Cilostazol Induces PGI2 Production via Activation of the Downstream Epac-1/Rap1 Signaling Cascade to Increase Intracellular Calcium by PLC? and to Activate p44/42 MAPK in Human Aortic Endothelial ... in PLoS ONE 2015
Results provide insight into the interrelationship between T-ALL oncogenic networks and the therapeutic efficacy of dual PI3Kgamma/delta inhibition in the context of NOTCH1 (show NOTCH1 Proteins) and cMYC (show MYC Proteins) signaling.
PIK3CG gene rs12667819 was shown to be associated with attention-deficit/hyperactivity disorder (ADHD) risk in dominant model, ADHD-I type, and symptom scores. Gene-environmental interactions analysis revealed potential interactions of rs12667819 collaborating with blood lead and feeding style to modify ADHD risk. Expression quantitative trait loci analysis suggested that rs12667819 may mediate PIK3CG gene expression.
Predicted activities were further evaluated through in-vitro testing of gallic acid and serpentine targeting PI3Kgamma.
PI3Kdelta and PI3Kgamma inhibition with IPI-145 has anti-proliferative activity in primary AML (show RUNX1 Proteins) cells by inhibiting the activity of AKT (show AKT1 Proteins) and MAPK (show MAPK1 Proteins)
we propose that the PKA-Smurf1 (show SMURF1 Proteins)-PIPKIgamma pathway has an important role in pulmonary tumorigenesis and imposes substantial clinical impact on development of novel diagnostic markers and therapeutic targets for lung cancer treatment.
A positive correlation may exist between PIK3CG single nucleotide polymorphisms and patients with poor responsiveness to clopidogrel.
PI3K (show PIK3CA Proteins), independently of protein kinase B (show AKT1 Proteins), has a role in parasite-induced netosis. One of the main isoforms involved is PI3Kgamma which works in a reactive-oxygen-species-dependent way.
Diminished expression of p110gamma in pulmonary vascular endothelial cells of patients with acute respiratory distress syndrome suggests that impaired p110gamma-FoxM1 vascular repair signaling is a critical factor in persistent leaky lung microvessels in ARDS.
Findings suggest the pathophysiological role of phosphoinositide 3-kinase gamma (PI3Kgamma) in atherogenesis.
Our findings suggest that p84 (show PPP1R12C Proteins) binding to p110gamma may represent a novel negative feedback signal that terminates PI3Kgamma activity.
As blockade of PI3Kgamma or integrin alpha4 prevents accumulation of myeloid-derived suppressor cells and reduces myeloid cell expression of immunosuppressive factors that stimulate tumor immune escape, these results highlight PI3Kgamma and integrin alpha4 as targets for the design of cancer therapeutics.
PI3K( PI3Kgamma(null) versus PI3Kgamma(WT) mice) inhibition slows tumor growth, enhances antitumor immunity, and heightens susceptibility to immune checkpoint inhibitors. We propose that combining PI3K inhibition with anti-PD1 (show PDCD1 Proteins) may be a viable therapeutic approach for triple-negative breast cancer
PI3Kg ablation protects mice from obesity, inflammation, and insulin (show INS Proteins) resistance caused by high-fat diet feeding.
The results showed that PI3K-gamma is likely a crucial element in sepsis-induced myocardial dysfunction (SIMD) by regulating the PI3K/Akt (show AKT1 Proteins) pathway, and become a new marker of myocardial injury. Inhibition of PI3K-gamma might be a potential therapeutic target in SIMD.
Phosphatidylinositol-3-kinases (PI3K) gamma and delta are key regulators of T cell signaling. Here the author show, using mouse heart allograft transplantation models, that PI3Kgamma or PI3Kdelta deficiency prolongs graft survival, but selective inhibition of PI3Kgamma or PI3Kdelta reveals alternative transplant survival outcomes post CTLA4 (show CTLA4 Proteins)-Ig treatment.
PI3Kgamma kinase activity-independent control of cAMP phosphodiesterase as a crucial mediator of microglial cAMP regulation, MMP-9 (show MMP9 Proteins) expression, and phagocytic activity following focal brain ischemia/recirculation.
We report here that PI3Kgamma regulates macrophage transcriptional programming, leading to T-cell suppression, desmoplasia, and metastasis in pancreas adenocarcinoma.
a STOP mutation in the GM-CSFRalpha (show CSF2RA Proteins) chain, leading to a complete and specific deficiency in GM-CSF (show CSF2 Proteins) signaling, is reported.
increased levels of eosinophils and IgE in p110gamma/delta-/- mice do not abolish the protective effect of p110gamma/delta-deficiency against OVAlbumin (show OVA Proteins)-induced allergic airway inflammation.
The Effector PI3Kgamma Is Required for Toll (show TLR4 Proteins)-like Receptors-induced Akt (show AKT1 Proteins)/mTOR (show FRAP1 Proteins) Signaling and Regulation of Cytokine Responses.
In conclusion, our observations reveal that PRRSV triggers the activation of FAK-PI3K-AKT-Rac1 signaling pathway to facilitate its entry into cells.
CSF2 (show CSF2 Proteins) stimulates proliferation of trophectoderm cells by activation of the PI3K-and ERK1/2 MAPK (show MAPK1 Proteins)-dependent MTOR (show FRAP1 Proteins) signal transduction cascades.
A linear relationship of EGF/EGFR (show EGFR Proteins), PI3-kinase (show PIK3CA Proteins), MAPK (show MAPK1 Proteins) and geminal vesicle breakdown, presents a relatively definitive mechanism of EGF (show EGF Proteins)-induced meiotic resumption of porcine oocyte.
This gene encodes a protein that belongs to the pi3/pi4-kinase family of proteins. The gene product is an enzyme that phosphorylates phosphoinositides on the 3-hydroxyl group of the inositol ring. It is an important modulator of extracellular signals, including those elicited by E-cadherin-mediated cell-cell adhesion, which plays an important role in maintenance of the structural and functional integrity of epithelia. In addition to its role in promoting assembly of adherens junctions, the protein is thought to play a pivotal role in the regulation of cytotoxicity in NK cells. The gene is located in a commonly deleted segment of chromosome 7 previously identified in myeloid leukemias.
, PI3-kinase subunit gamma
, phosphatidylinositol 3 kinase gamma, p110 gamma
, phosphatidylinositol 3-kinase catalytic 110-kD gamma
, phosphatidylinositol 3-kinase, catalytic, gamma polypeptide
, phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit gamma
, phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit gamma isoform
, phosphatidylinositol-4,5-bisphosphate 3-kinase 110 kDa catalytic subunit gamma
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma isoform
, phosphoinositide-3-kinase gamma catalytic subunit
, phosphoinositide-3-kinase, catalytic, gamma polypeptide
, ptdIns-3-kinase subunit gamma
, ptdIns-3-kinase subunit p110-gamma
, serine/threonine protein kinase PIK3CG
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma isoform-like
, catalytic subunit of G-beta-gamma-activated
, phosphoinositide-3-kinase catalytic gamma polypeptide