抗Human PIK3CG 抗体:
抗Rat (Rattus) PIK3CG 抗体:
抗Mouse (Murine) PIK3CG 抗体:
Human Polyclonal PIK3CG Primary Antibody for ELISA, WB - ABIN545105
Osaki, Kase, Adachi, Takeda, Hashimoto, Ito: Inhibition of the PI3K-Akt signaling pathway enhances the sensitivity of Fas-mediated apoptosis in human gastric carcinoma cell line, MKN-45. in Journal of cancer research and clinical oncology 2003
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Human Polyclonal PIK3CG Primary Antibody for IHC (p), ELISA - ABIN544996
Andreozzi, DAlessandris, Federici, Laratta, Del Guerra, Del Prato, Marchetti, Lauro, Perticone, Sesti et al.: Activation of the hexosamine pathway leads to phosphorylation of insulin receptor substrate-1 on Ser307 and Ser612 and impairs the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin ... in Endocrinology 2004
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Human Polyclonal PIK3CG Primary Antibody for IHC (p), ELISA - ABIN544995
Reddy, Lin, Huang, Samanta, Liao: The IL-1 receptor accessory protein is essential for PI 3-kinase recruitment and activation. in Biochemical and biophysical research communications 2004
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Human Polyclonal PIK3CG Primary Antibody for IHC (p), ELISA - ABIN544176
Chandrasekar, Mohanam, Gujrati, Olivero, Dinh, Rao: Downregulation of uPA inhibits migration and PI3k/Akt signaling in glioblastoma cells. in Oncogene 2003
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Human Polyclonal PIK3CG Primary Antibody for WB - ABIN6672115
Huang, Cao, Ou, Yang, Zheng, Tang, Chen, Hu, Zheng, Wang: The long non-coding RNA PTTG3P promotes cell growth and metastasis via up-regulating PTTG1 and activating PI3K/AKT signaling in hepatocellular carcinoma. in Molecular cancer 2018
The results demonstrated that the MIR31HG-miR-31-ITIH5-PIK3CG pathway plays a role in the pathogenesis of Hirschsprung disease.
Circulating exosomal miR-301a-3p levels positively associated with depth of invasion, lymph node metastasis, late TNM stage, and poor prognosis of pancreatic cancer. Hypoxic exosomal miR-301a-3p induced the M2 polarization of macrophages via activation of the PTEN/PI3Kgamma signaling pathway.
SNPs rs17847825 and rs2230460 significantly associated with protection from severe disease using the recessive model in patients infected with influenza A(H1N1)pdm09.
a novel role for GRK2 as a target of TCR signaling that is responsible for TCR-induced transactivation of CXCR4 and TCR-CXCR4 complex formation that signals via PI3Kgamma/PREX1 to mediate cytokine production.
High PIK3CG expression correlates with low parasitism in human chagasic hearts. These data identify a previously unrecognized role of the canonical PI3Kgamma signaling pathway in the control of T. cruzi infection.
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 and cMYC 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 cells by inhibiting the activity of AKT and MAPK
we propose that the PKA-Smurf1-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, independently of protein kinase B, 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 binding to p110gamma may represent a novel negative feedback signal that terminates PI3Kgamma activity.
findings suggest that miR-502 functions as a tumor suppressor in HCC via inhibition of PI3KCG, supporting its utility as a promising therapeutic gene target for this tumor type
PI3Kgamma plays an important role in the development of eosinophilic inflammation a
PI3Kgamma-induced VEGF expression was reduced when the human tocopherol-associated protein 1 (hTAP1/SEC14L2) was overexpressed suggesting formation of an inactive PI3Kgamma/hTAP1 heterodimer.
data argue for differential regulatory functions of the non-catalytic subunits and a specific Gbetagamma-dependent regulation of p101 in PI3Kgamma activation.
The interaction between PI3Kgamma and CNGA1 does not appear to play a role in regulation of CNG channel activity, but PI3Kgamma uses CNGA1 as an anchoring module to achieve close proximity to its substrate to generate D3-phosphoinositides
PI3Kgamma aggravates the progression of early tuberculosis infection and reduces the frequency of CD4+IL-17+ cells, the production of IL-17 ex vivo as well as gene and protein expression of molecules associated with Th17 cell differentiation.
the lack of PI3Kgamma favors M1 macrophages polarization providing an inflammatory-prone environment, which does not prevent kidney diseases progression.
Deficient mice in the canonical PI3Kgamma signaling (Pik3cg-/-) are more susceptible to T. cruzi infection. The canonical PI3Kgamma signaling in myeloid cells restricts heart parasitism and avoids heart damage and death of mice.
the beneficial action of PI3Kgamma ablation in obesity-driven glucose intolerance is largely a result of its leptin-dependent effects on adiposity and, to a lesser extent, the promotion of adipose tissue neutrophil recruitment and M1 polarization of gene expression
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 may be a viable therapeutic approach for triple-negative breast cancer
PI3Kg ablation protects mice from obesity, inflammation, and insulin 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 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-Ig treatment.
PI3Kgamma kinase activity-independent control of cAMP phosphodiesterase as a crucial mediator of microglial cAMP regulation, MMP-9 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 chain, leading to a complete and specific deficiency in GM-CSF 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-induced allergic airway inflammation.
The Effector PI3Kgamma Is Required for Toll-like Receptors-induced Akt/mTOR Signaling and Regulation of Cytokine Responses.
macrophage PI 3-kinase gamma controls a critical switch between immune stimulation and suppression during inflammation and cancer; therapeutic targeting of intracellular signalling pathways that regulate the switch between macrophage polarization states can control immune suppression in cancer and other disorders
Accumulation of PtdIns(3,4,5)P3, but not PtdIns(3,4)P2,in neutrophils were dependent on PI3Kgamma activity.
identify PI3Kgamma as a novel key host protective factor in influenza virus infection and shed light on an unappreciated layer of complexity concerning the role of PI3K signaling in this context
Pik3cg(-/-) mice had persistent lung inflammation induced by sepsis and increased in vascular permeability. Restoration of p110gamma in pulmonary endothelial cellsrestored endothelial regeneration and normalized the defective vascular repair program.
Results found that the absence of PI3Kgamma significantly delayed mortality and reduced clinical signs and histopathological brain changes associated with Plasmodium berghei infection.
The authors demonstrate that the Attention Deficit Disorder with Hyperactivity phenotype depends on a dysregulation of CREB signaling exerted by a kinase-independent PI3Kgamma-PDE4D interaction in the noradrenergic neurons of the locus coeruleus.
In conclusion, our observations reveal that PRRSV triggers the activation of FAK-PI3K-AKT-Rac1 signaling pathway to facilitate its entry into cells.
CSF2 stimulates proliferation of trophectoderm cells by activation of the PI3K-and ERK1/2 MAPK-dependent MTOR signal transduction cascades.
A linear relationship of EGF/EGFR, PI3-kinase, MAPK and geminal vesicle breakdown, presents a relatively definitive mechanism of EGF-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