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NOS3 — PIK3CA
Text-mined interactions from Literome
Thomas et al., J Biol Chem 2002
(Calcium Signaling) :
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
Rikitake et al., Arterioscler Thromb Vasc Biol 2002
:
S1P activated the phosphatidylinositol-3-kinase (PI3K)/Akt/endothelial NO synthase (eNOS) pathway in ECs, since S1P stimulated
eNOS phosphorylation and NO production were
blocked by inhibition of activities of
PI3K and Akt
Boo et al., Am J Physiol Heart Circ Physiol 2002
:
These results suggest that shear stress stimulates
eNOS by two different mechanisms : 1 ) PKA- and
PI3K dependent and 2 ) PKA dependent but PI3K independent pathways
Kristof et al., J Biol Chem 2003
(Inflammation) :
The
role of mTOR and
PI3K in the activation of human inducible
nitric oxide synthase transcription by cytokines and lipopolysaccharide (LPS) was investigated in lung epithelial adenocarcinoma ( A549 ) cells
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
Papapetropoulos et al., Mol Pharmacol 2004
:
In addition, wortmannin, a
PI3-K inhibitor,
blocked both the vanadate induced phosphorylation of
eNOS and the increase in cGMP accumulation
Slomiany et al., IUBMB Life 2004
(Gastritis...) :
Our findings suggest that PAF, through the interference with
PI3K dependent
cNOS activation, plays a critical role in influencing the extent of pathological consequences of H. pylori infection on the synthesis of gastric mucin
Ortiz et al., American journal of physiology. Renal physiology 2004
:
In other cells,
eNOS activation by shear stress is
mediated by
phosphatidylinositol 3-OH kinase (PI3)-kinase
Jia et al., J Biol Chem 2004
:
VEGF-D induced strong but more transient phosphatidylinositol 3-kinase (PI3K) mediated Akt activation and increased
PI3K dependent endothelial
nitric-oxide synthase phosphorylation and cell survival more weakly
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
Namkoong et al., Exp Mol Med 2005
:
These results clearly show that PGE2 increased angiogenesis by activating the NO/cGMP signaling pathway through
PKA/PI3K/Akt dependent increase in
eNOS activity
Sun et al., Toxicol Appl Pharmacol 2006
:
Serine 1179 phosphorylation of endothelial
nitric oxide synthase caused by 2,4,6-trinitrotoluene through
PI3K/Akt signaling in endothelial cells
Lee et al., Am J Physiol Heart Circ Physiol 2006
(Inflammation...) :
The
PI3K inhibitor and a dominant negative mutant of Akt
suppressed Akt and
eNOS phosphorylation and NO production
Kim et al., Biol Pharm Bull 2007
:
Water extract of Korean red ginseng stimulates angiogenesis by activating the
PI3K/Akt dependent ERK1/2 and
eNOS pathways in human umbilical vein endothelial cells ... Inhibition of
PI3K activity by wortmannin completely
inhibited KRGE induced angiogenesis and phosphorylation of Akt, ERK1/2, and
eNOS , indicating that PI3K/Akt activation is an upstream event of the KRGE mediated angiogenic pathway ... This study demonstrated that KRGE stimulates in vitro and in vivo angiogenesis through the activation of the
PI3K/Akt dependent ERK1/2 and
eNOS signal pathways and their cross talk
Chung et al., Biochem Biophys Res Commun 2008
(MAP Kinase Signaling System) :
The
PI3K inhibitor Wortmannin
suppressed icariin mediated angiogenesis and Akt and
eNOS activation without affecting ERK phosphorylation
Martinelli et al., Mol Biol Cell 2009
:
In particular, phosphorylation of
eNOS on S1177 in response to ICAM-1 activation was
regulated by src family protein kinase, rho GTPase, Ca ( 2+ ), CaMKK, and AMPK, but not
Akt/PI3K
Ramella et al., J Cell Biochem 2010
:
These results suggest a novel signal transduction pathway for endogenous cationic and amphipathic peptides in endothelial cells : HSPGs interaction and caveolae endocytosis, coupled with a
PI3K dependent
eNOS phosphorylation
Wang et al., Am J Physiol Heart Circ Physiol 2010
(Disease Models, Animal...) :
Importantly, inhibition of either
PI3K or eNOS attenuated exercise induced restoration of the dilatation function and
blocked PI3K, Akt, and
eNOS phosphorylation by ACh in the mesenteric arteries
Ramella et al., Regul Pept 2011
:
Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce
PI3K/Akt dependent
eNOS phosphorylation and NO release
Makarova et al., J Biol Chem 2011
(Acute Lung Injury...) :
uPA induced phosphorylation of
eNOS was also inhibited by the protein kinase A (PKA) inhibitor, myristoylated PKI, but was not
dependent on
PI3K-Akt signaling
Wen et al., FASEB J 2011
:
Overall, using biochemical, cellular, genetic, and physiological approaches, our findings reveal that adenosine is a novel molecule signaling via A ( 2B ) R activation, contributing to penile erection via
PI3K/AKT dependent
eNOS activation
Maeno et al., J Biol Chem 2012
(Metabolic Diseases) :
Thus, PKC and angiotensin induced phosphorylation of Thr-86 of
p85/PI3K may partially
inhibit the activation of
PI3K/eNOS by multiple cytokines and contribute to endothelial dysfunction in metabolic disorders
Li et al., J Vasc Surg 2012
(Carotid Stenosis...) :
Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing
PI3K/Akt dependent
Hsp70/eNOS signaling
Park et al., Vascul Pharmacol 2012
:
These effects of GJ were attenuated not only by calcium chelators including EGTA and BAPTA-AM, but also by LY294002, a PI3K/Akt inhibitor, indicating calcium- and
PI3K/Akt dependent
activation of
eNOS by GJ
Coso et al., PloS one 2012
:
Furthermore, activation of
PI3K/Akt by VEGF-C/VEGFR-3
resulted in phosphorylation of P70S6K,
eNOS , PLC?1, and Erk1/2
Liu et al., Brain Res Bull 2012
(Brain Ischemia...) :
Losartan, an angiotensin II type 1 receptor blocker, ameliorates cerebral ischemia-reperfusion injury via
PI3K/Akt mediated
eNOS phosphorylation
Haeussler et al., J Biol Chem 2013
:
Knockdown of H-Ras blocked VEGF induced
PI3K dependent Akt ( Ser-473 ) and
eNOS ( Ser-1177 ) phosphorylation and nitric oxide dependent cell migration, demonstrating the essential role of H-Ras
Trott et al., Eur J Appl Physiol 2013
:
Collectively, these results indicate that impaired NO-mediated, endothelium dependent dilation in old SFA is due, in part, to an impaired potential for
PI3K/Akt dependent phosphorylation of
eNOS on ser ( 1177 )
Hu et al., PloS one 2013
:
Although stretch activated the kinases AMPKa, PKA, Akt, and ERK1/2, stretch induced
eNOS activation was only
inhibited by kinase-specific inhibitors of PKA and
PI3K/Akt , but not of AMPKa and Erk1/2