Aperçu des produits pour anti-PIK3CG (PIK3CG) Anticorps

Human Phosphoinositide-3-Kinase, Catalytic, gamma Polypeptide (PIK3CG) interaction partners

1. SNPs rs17847825 and rs2230460 significantly associated with protection from severe disease using the recessive model in patients infected with influenza A(H1N1)pdm09.

2. 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.

3. 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.

4. 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.

5. 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.

6. Predicted activities were further evaluated through in-vitro testing of gallic acid and serpentine targeting PI3Kgamma.

7. PI3Kdelta and PI3Kgamma inhibition with IPI-145 has anti-proliferative activity in primary AML cells by inhibiting the activity of AKT and MAPK

8. 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.

9. A positive correlation may exist between PIK3CG single nucleotide polymorphisms and patients with poor responsiveness to clopidogrel.

10. 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.

11. 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.

12. Findings suggest the pathophysiological role of phosphoinositide 3-kinase gamma (PI3Kgamma) in atherogenesis.

13. Our findings suggest that p84 binding to p110gamma may represent a novel negative feedback signal that terminates PI3Kgamma activity.

14. 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

15. PI3Kgamma plays an important role in the development of eosinophilic inflammation a

16. 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.

17. data argue for differential regulatory functions of the non-catalytic subunits and a specific Gbetagamma-dependent regulation of p101 in PI3Kgamma activation.

18. 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

19. Mfng is an oncogene acting through Notch-mediated induction of Pik3cg.

20. increased susceptibility of individuals with COPD to influenza likely results from impaired antiviral responses, which are mediated by increased PI3K-p110alpha activity.

Mouse (Murine) Phosphoinositide-3-Kinase, Catalytic, gamma Polypeptide (PIK3CG) interaction partners

1. 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.

2. the lack of PI3Kgamma favors M1 macrophages polarization providing an inflammatory-prone environment, which does not prevent kidney diseases progression.

3. 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.

4. 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

5. 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.

6. 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

7. PI3Kg ablation protects mice from obesity, inflammation, and insulin resistance caused by high-fat diet feeding.

8. 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.

9. 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.

10. 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.

11. We report here that PI3Kgamma regulates macrophage transcriptional programming, leading to T-cell suppression, desmoplasia, and metastasis in pancreas adenocarcinoma.

12. a STOP mutation in the GM-CSFRalpha chain, leading to a complete and specific deficiency in GM-CSF signaling, is reported.

13. 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.

14. The Effector PI3Kgamma Is Required for Toll-like Receptors-induced Akt/mTOR Signaling and Regulation of Cytokine Responses.

15. 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

16. Accumulation of PtdIns(3,4,5)P3, but not PtdIns(3,4)P2,in neutrophils were dependent on PI3Kgamma activity.

17. 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

18. 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.

19. Results found that the absence of PI3Kgamma significantly delayed mortality and reduced clinical signs and histopathological brain changes associated with Plasmodium berghei infection.

20. 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.

Pig (Porcine) Phosphoinositide-3-Kinase, Catalytic, gamma Polypeptide (PIK3CG) interaction partners

1. In conclusion, our observations reveal that PRRSV triggers the activation of FAK-PI3K-AKT-Rac1 signaling pathway to facilitate its entry into cells.

2. CSF2 stimulates proliferation of trophectoderm cells by activation of the PI3K-and ERK1/2 MAPK-dependent MTOR signal transduction cascades.

3. 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.