Ignet

Gene Information

Gene symbol: PIK3CG

Gene name: phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma

HGNC ID: 8978

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	AKT1	1 hits
3	BECN1	1 hits
4	CTGF	1 hits
5	H2AFX	1 hits
6	HPSE	1 hits
7	HSPA1A	1 hits
8	IGF1	1 hits
9	IL4	1 hits
10	INS	1 hits
11	INSR	1 hits
12	IRS1	1 hits
13	IRS2	1 hits
14	MAP3K14	1 hits
15	MAPK1	1 hits
16	MCM7	1 hits
17	MTTP	1 hits
18	MYH14	1 hits
19	NOS3	1 hits
20	PI3	1 hits
21	PIGU	1 hits
22	PIK3CA	1 hits
23	PIK3R1	1 hits
24	PLD1	1 hits
25	POMC	1 hits
26	PPP1R12A	1 hits
27	PRKCA	1 hits
28	PTPN11	1 hits
29	RHOD	1 hits
30	SLC2A1	1 hits
31	SLC2A4	1 hits
32	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	1380456	Furthermore, overexpression of IRS-1 potentiates the activation of PtdIns 3-kinase in insulin-stimulated cells, and tyrosyl phosphorylated IRS-1 or peptides containing phosphorylated YXXM motifs activate PtdIns 3'-kinase in vitro.
2	8385139	Overexpression of IRS-1 in CHO cells increases the amount of PtdIns 3'-kinase activity in alpha IR immunoprecipitates, and IRS-1 markedly increases the in vitro binding of p85 alpha and PtdIns 3-kinase activity to anti-receptor immunoprecipitates.
3	7686165	Overexpression of the insulin receptor increased sensitivity of glucose uptake and the maximal response of PI3 kinase activation to insulin.
4	7686165	Overexpression of the IGF-I receptor did not affect sensitivity or maximal responsiveness of glucose uptake or PI3 kinase activation to IGF-I.
5	10976915	Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation.
6	10976915	We conclude that insulin stimulates MBP via its regulatory subunit, MBS partly by inactivating Rho kinase and stimulating NO/cGMP signaling via PI3-kinase as part of a complex signaling network that controls 20-kDa myosin light chain (MLC20) phosphorylation and VSMC contraction.
7	10989952	It generates insulin-like signals for glucose transport and glycogen synthesis via leptin receptors and the PI3-kinase and could, therefore, play a role as a mediator of obesity-related insulin resistance.
8	11018037	VEGF activated the tyrosine receptor phosphorylation of KDR and Flt1 and increased the binding of phosphatidylinositol 3-kinase (PI3-kinase) p85 subunit to KDR and Flt1, both of which could mediate CTGF gene induction.
9	11018037	VEGF-induced CTGF expression was mediated primarily by PI3-kinase activation, whereas PKC and ERK pathways made only minimal contributions.
10	11739394	Hypertension (in spontaneous hypertensive rats) or expression of an active RhoA(V14) up-regulates Rho kinase activity and increases ROK-alpha/IRS-1 association resulting in IRS-1 serine phosphorylation that leads to inhibition of both insulin-induced IRS-1 tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3-kinase) activation.
11	11739394	In contrast, expression of dominant negative RhoA or cGMP-dependent protein kinase type I alpha inactivates Rho kinase, abolishes ROK-alpha/IRS-1 association, and potentiates insulin-induced tyrosine phosphorylation and PI3-kinase activation leading to decreased MBS(T695) phosphorylation and decreased MBP inhibition.
12	11916925	This insulin resistance was associated with impaired insulin receptor substrate (IRS)-2-associated phosphatidylinositol 3' (PI3) kinase activation and IRS-2 tyrosine phosphorylation as well as significantly decreased protein kinase C (PKC)-zeta/lambda activation in response to insulin.
13	14516785	The p38MAPK inhibitor SB203580, the phosphatidylinositol 3 kinase (PI3-kinase) pathway inhibitor wortmannin, and the protein kinase C pathway (PKC) inhibitor G� 6976 did not significantly affect mitogen-induced MCM6 and MCM7 expression.
14	14551245	Because chronic insulin can increase the levels of phosphatidylinositol 3 (PI3) kinase in several models of hyperinsulinemia, we also tested the potential involvement of this enzyme in mechanisms leading to increased cell motility.
15	14551245	We found that the motogenic effect of NO, Gab1, and SHP2 was blocked by the selective PI3 kinase inhibitor LY294002, suggesting a requirement of PI3 kinase in mediating motogenesis.
16	15526284	LY294002, a phosphatidylinositol 3 (PI3) kinase inhibitor, inhibited the association of eNOS/Akt and the phosphorylation of eNOS but had no effect on the interaction between eNOS and HSP90 during early hours of exposure.
17	15386812	Signaling-related defects in the soleus muscle of sedentary obese Zucker rats, which impaired glucose transporter subtype 4 (GLUT 4), included decreased phosphorylation of insulin receptor substrate (IRS)-1, as well as an attenuated p85 regulatory subunit of phosphatidylinositol 3-kinase (PI3 kinase) and Akt serine phosphorylation.
18	15386812	Enhanced insulin sensitivity via exercise training might be mediated by endogenous beta-endorphin through an increase of postreceptor insulin signaling related to the IRS-1-associated PI3-kinase step that leads to the enhancement of GLUT 4 translocation and improved glucose disposal in obese Zucker rats.
19	16354680	These serines lie close to the Y(632)MPM motif that is implicated in the binding of p85alpha/p110alpha PI3-kinase to IRS-1 upon insulin stimulation.
20	16354680	Phosphomimicking mutations of these serines block insulin-stimulated activation of IRS-1-associated PI3-kinase.
21	16873703	In response to hyperthermia, the activation of serine/threonine kinase Akt depending on phosphatidylinositol 3 (PI3) kinase was necessary for cardiac expression of HSP72.
22	18207474	DAG is identified as a potential mediator of lipid-induced insulin resistance, as increased DAG levels are associated with protein kinase C activation and a reduction in both insulin-stimulated IRS-1 tyrosine phosphorylation and PI3 kinase activity.
23	18779578	Up-regulation of insulin-like growth factor 1 (IGF-1) expression and plasma levels and increasing IGF-1 receptor phosphorylation in muscle may explain the increased insulin receptor substrate 1, PI3K, and ERK phosphorylation in skeletal muscle.
24	19915586	Insulin mediates Na(+)/K(+)-ATPase alpha1- and alpha2-subunit translocation to the cardiac muscle plasma membrane via a PI3-kinase-dependent mechanism.
25	19917066	EPCs isolated from healthy adults were cultured with various concentrations of AGEs (0, 50, 100 and 200 mg L(-1)) with or without rosiglitazone (10 nM), antibody for the receptors for AGE-human serum albumin (anti-receptor for advanced glycation end products (RAGE); 50 microg mL(-1)), phosphatidylinositol-3-kinase (PI3K) inhibitor (LY294002, 5 microM), nitric oxide (NO) synthase inhibitor (L-N(G)-nitro-arginine methyl ester (L-NAME), 100 microM) or sodium nitroprusside (SNP, 25 microM).
26	19531027	In support of this, Western blotting revealed that incubation of cells with IL-4 resulted in increased phosphorylation of Akt (also called protein kinase B), a downstream target of PI3K.
27	19531027	We conclude that IL-4 receptors are functionally competent in pancreatic beta-cells and that they signal via PI3K and JAK/STAT pathways.
28	19944677	Both young and adult SHRs showed significant downregulated expression of PI3-kinase and decreased insulin-stimulated phosphorylations of Akt and eNOS in vascular tissues.
29	19373754	The PI3 kinase inhibitor LY 294002 blocked the increase in VEGF-A.
30	20045149	Influence of insulin (0.02 micromol/L) on isometric twitch force was examined with and without blocking glucose transporter (GLUT) 4 translocation (latrunculin), sodium-coupled glucose transporter (SGLT) 1 (phlorizin, T-1095A), or PI3-kinase (wortmannin).
31	20736911	This phosphorylation of H2AX is mediated by the phosphatidyl-inosito 3-kinase (PI3K) family of proteins, ataxia telangiectasia mutated (ATM), DNA-protein kinase catalytic subunit and ATM and RAD3-related (ATR).
32	20189175	Indeed, defective activation of PI3-kinase, secondary to insulin resistance, is associated with a reduction of apoB degradation in the hepatocytes, a rise in MTP expression (by increasing nuclear transcription factors Fox01 and Foxa2) and an increased activity of phospholipase D1 and ARF-1, which are involved in VLDL(1) formation.
33	21099282	The role and mechanism of phosphatidylinositol 3-OH (PI3) kinase as a regulator of insulin secretion is much debated.
34	21099282	More recent studies, including our own recently published work, have begun to investigate PI3 kinase isoform-specific mechanisms regulating insulin secretion.
35	21099282	Building on our previous work demonstrating that mice lacking a G-protein coupled PI3 kinase catalytic subunit (p110? -/-) lack first phase insulin secretion and display a blunted second phase of secretion, we have now elucidated the mechanism by which this PI3 kinase isoform acts as a positive regulator of insulin secretion.
36	21436039	Mice lacking p110? (Pik3cg(-/-)), the catalytic subunit of PI3K?, exhibited improved systemic insulin sensitivity with enhanced insulin signaling in the tissues of obese animals.
37	20712405	Among the proteins and multimolecular complexes that contribute to autophagosome formation are the PI(3)-binding proteins, the PI3-phosphatases, the Rab proteins, the Atg1/ULK1 protein-kinase complex, the Atg9?Atg2-Atg18 complex, the Vps34-Atg6/beclin1 class III PI3-kinase complex, and the Atg12 and Atg8/LC3 conjugation systems.
38	21354306	Inhibition of PI3-kinase reversed this protective effect of IRS-1 or IRS-2.
39	21646544	Pharmacological and genetic interventions revealed that insulin regulates GLUT4 and FoxO1 through the PI3-kinase isoform p110?, although FoxO1 showed higher sensitivity to p110? activity than GLUT4.
40	21646544	Transient down-regulation and overexpression of Akt isoforms in adipocytes demonstrated that insulin-activated PI3-kinase signals to GLUT4 primarily through Akt2 kinase, whereas Akt1 and Akt2 signal to FoxO1.
41	21461610	Moreover, pretreatment with inhibitors of nuclear factor-?B (NF-?B) or PI3-kinase did not affect heparanase expression induced by AGE-BSA.
42	21846802	The decrease in insulin-stimulated glucose uptake was associated with a significant decrease in PI3 kinase activity and protein kinase B/Akt phosphorylation.
43	21846802	Adiponectin treatment inhibited NIK-induced NF-?B activation and restored insulin sensitivity by restoring PI3 kinase activation and subsequent Akt phosphorylation.
44	16443776	Phosphatidylinositol 3-kinase (PI3 kinase) inhibition disrupts the ability of insulin to stimulate GLUT1 and GLUT4 translocation into the cell membrane and thus glucose transport.
45	21786209	In addition, betel nut extract and arecoline increased the basal level of IRS-1 serine(307) phosphorylation and decreased insulin-stimulated IRS-1 tyrosine, Akt, and PI3 kinase phosphorylation.