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NOS3 — PI3

Text-mined interactions from Literome

Isenović et al., Biochem Biophys Res Commun 2001 : Role of PI3-kinase in isoproterenol and IGF-1 induced ecNOS activity
Thomas et al., J Biol Chem 2002 (Calcium Signaling) : H ( 2 ) O ( 2 ) -induced promotion of eNOS activity and modulation of the eNOS phosphorylation status at Ser-1177 and Thr-495 were significantly attenuated by selective inhibitors of Src kinase, the ErbB receptor family, and phosphoinositide 3-kinase (PI 3-K) ... In turn, PI 3-K mediates eNOS Ser-1177 phosphorylation via a calcium- and Akt dependent pathway, whereas eNOS Thr-495 dephosphorylation does not involve calcium or Akt
Souza et al., Mol Med 2001 (MAP Kinase Signaling System) : PI-3-kinase inhibitors, Wortmannin and LY294002 inhibited arsenite induced phosphorylation of AKT and eNOS but had no effect on phosphorylation of p38
Hurt et al., Proc Natl Acad Sci U S A 2002 : Our findings support a model in which rapid, brief activation of neuronal NOS initiates the erectile process, whereas PI3-kinase/Akt dependent phosphorylation and activation of eNOS leads to sustained NO production and maximal erection
Kou et al., Biochemistry 2002 : In BAEC, activation of eNOS by LPA is completely blocked by pertussis toxin, by the intracellular calcium chelator BAPTA ( 1,2-bis ( aminophenoxy ) ethane-N, N,N ', N'-tetraacetic acid ), and by the phosphoinositide 3-kinase (PI3-K) inhibitor wortmannin, but is unaffected by U0126, an inhibitor of mitogen activated protein ( MAP ) kinase pathways
Park et al., J Korean Med Sci 2002 (MAP Kinase Signaling System) : This suggests that eNOS expression might be regulated by PI-3K and the ERK1/2 signaling pathway ... In addition, eNOS may be regulated by the PI-3K or mitogen activated protein kinase pathway
Lau et al., Chang Gung Med J 2002 : Recent investigations have shown that estrogen 's rapid stimulatory action on eNOS is mediated by the activation of phosphatidylinositol 3-kinase (PI3-K) and protein kinase B (PKB)/Akt pathway among other signaling systems
Babaei et al., Am J Pathol 2003 : In summary, our results demonstrate for the first time that endothelial derived NO is required for Ang1 induced angiogenesis, and that the PI3-kinase signaling mediates the activation of eNOS and NO release in response to Ang1
Mukai et al., J Cardiovasc Pharmacol 2003 : Western blot analysis showed that the extent of phosphorylation of Akt, an active form of Akt, was increased by cerivastatin while it was reduced by LY294002, suggesting an involvement of PI3 kinase/Akt dependent activation of endothelial NOS
Liu et al., Circulation 2003 (MAP Kinase Signaling System) : In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K) dependent increase in nitric oxide synthase activity as well as PI3K dependent activation of extracellular signal regulated kinase 1/2 and p70 S6 kinase
Ortiz et al., American journal of physiology. Renal physiology 2004 : We next studied which PI3-kinase product mediates eNOS translocation
Herrera et al., American journal of physiology. Renal physiology 2004 : In nonrenal tissue, chronic exposure to ET-1 stimulates eNOS expression via the ET ( B ) receptor and activation of phosphatidylinositol 3-kinase (PI3K)
Budzyn et al., J Pharmacol Exp Ther 2005 (Hypertension...) : Phosphatidylinositol 3-kinase (PI3K) can activate endothelial nitric oxide synthase (eNOS) , leading to production of the vasodilator NO
Urbich et al., Kidney Int 2005 (Coronary Artery Disease) : At the molecular level, these factors are well established to activate the phosphatidyl-inositol-3-kinase (PI3K)-Akt dependent activation of the endothelial nitric oxide synthase (eNOS) , suggesting that the PI3K-Akt-eNOS signaling pathway may be involved in the transduction of atheroprotective factors
Kim et al., J Mol Cell Cardiol 2005 : Since activation of endothelial nitric oxide synthase (eNOS) is dependent on IRS-1/PI3-kinase signaling, we hypothesized that activation of IKKbeta may contribute to the effect of glucose to impair NO production
Li et al., Endothelium : journal of endothelial cell research 2005 : In conclusion, pulsatile shear stress greatly induces NO production by OFPAE cells through the mechanisms of both PI-3K mediated eNOS activation and elevations in eNOS protein levels ; bFGF does not further stimulate eNOS expression under flow condition
Kasina et al., Nitric Oxide 2006 : A decrease in the level of nitroprofilin in PDBu treated platelets in the presence of inducible nitric oxide synthase inhibitor, 1400W, was observed suggesting that profilin nitration is mediated by PI 3-kinase dependent activation of inducible nitric oxide synthase
Chen et al., Sci China C Life Sci 2005 : Results show that both exogenous and endogenous EETs could remarkably enhance eNOS expression and its phosphorylation at Ser1179 and Thr497 residues ; PI3K inhibitor LY294002 could inhibit EETs induced increase in eNOS-Ser ( P ) 1179 but had no effect on the change of eNOS-Thr ( P ) 497, while Akt inhibitor could attenuate the increase in phosphor-eNOS at both residues ; both of the two inhibitors could block EETs enhanced eNOS expression
Anselm et al., Cardiovasc Res 2007 : In addition, CGJ induced NO formation is due to the redox-sensitive activation of Src kinase with the subsequent PI3-kinase/Akt dependent phosphorylation of eNOS
Eva et al., Biochim Biophys Acta 2006 : Our findings indicate that ouabain, applied at low concentrations to human umbilical cord endothelial cells ( HUAECs ), induces a reaction cascade that leads to translocation of endothelial nitric oxide synthase (eNOS) and to activation of phosphatidylinositol 3-kinase (PI3K)
Jiang et al., Prostaglandins Other Lipid Mediat 2007 (MAP Kinase Signaling System) : Inhibition of phosphatidylinositol 3-kinase (PI3K) with LY294002 prevented EETs induced increases of eNOS-Ser ( P ) 1179 but had no effect on the phosphorylation status of Thr497
Yu et al., Biochem Biophys Res Commun 2007 : The results suggest that PI3kinase/Akt and MEK/ERK pathways and androgen receptor are involved in the regulation of acute eNOS activation by Rb1 in human aortic endothelial cells
Nakaya et al., J Med Invest 2007 : SH-6 ( 10 microM ), an Akt inhibitor, and wortmannin, a PI3-kinase inhibitor, completely blocked activation of K ( Ca ) channels by ginsenoside Re, indicating that it activates eNOS via a c-Src/PI3-kinase/Akt dependent mechanism
Cattaneo et al., Br J Pharmacol 2008 : We also found that oxytocin stimulates the phosphorylation of endothelial nitric oxide synthase (eNOS) via the phosphatidylinositol-3-kinase (PI-3-K)/AKT pathway, and that the activation of PI-3-K and formation of nitric oxide ( NO ) are required for the pro-migratory effect of oxytocin
Kaiserova et al., J Biol Chem 2008 (Myocardial Reperfusion Injury) : Treatment with bradykinin and insulin led to a phosphatidylinositol 3-kinase (PI3K) dependent increase in the phosphorylation of endothelial NOS at Ser-1177 and, even in the absence of ischemia, was sufficient in activating AR. Activation of AR by bradykinin and insulin was reversed upon reduction with dithiothreitol or by inhibiting NOS or PI3K
Downey et al., Ann N Y Acad Sci 2008 (Myocardial Ischemia) : PI3-kinase causes extracellular signal regulated kinase ( ERK ) -dependent activation of endothelial nitric oxide synthase
Yu et al., Endocrinology 2010 : The rapid phosphorylation of eNOS or NO production induced by testosterone was inhibited by Akt inhibitor SH-5 or by phosphatidylinositol (PI) 3-kinase inhibitor wortmannin ... Activation of PI3-kinase/Akt signaling and the direct interaction of AR with p85alpha are involved , at least in part, in eNOS phosphorylation
Auger et al., Mol Nutr Food Res 2010 : Phenolic extracts from red wine ( RWPs ) have been shown to induce nitric oxide ( NO ) -mediated vasoprotective effects, mainly by causing the PI3-kinase/Akt dependent activation of endothelial NO synthase (eNOS)
Kurita et al., Food Funct 2013 (Cardiovascular Diseases) : ( - ) -Epigallocatechin-3-O-gallate ( EGCg ) has been shown to induce endothelium dependent nitric oxide ( NO ) -mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt dependent phosphorylation of endothelial NO synthase (eNOS)
Alhosin et al., PloS one 2013 : Redox-Sensitive Up-Regulation of eNOS by Purple Grape Juice in Endothelial Cells : Role of PI3-Kinase/Akt , p38 MAPK, JNK, FoxO1 and FoxO3a
Malek et al., Biochem Biophys Res Commun 1999 : However, eNOS mRNA upregulation was potentiated by the PI 3-kinase inhibitors wortmannin and LY294002, suggesting that PI 3-kinase inhibits the shear response