PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28138348-0 2017 Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation & Shear Stress-Induced NO Production. Cholesterol 0-11 nitric oxide synthase 3 Homo sapiens 59-63 28831159-6 2017 HMG Co-A reductase negatively regulates eNOS, and the PLD2-deficiency phenotype of decreased eNOS expression and activity could be rescued by cholesterol supplementation and HMG Co-A reductase inhibition. Cholesterol 142-153 nitric oxide synthase 3 Homo sapiens 93-97 28138348-7 2017 Our results show that cholesterol enrichment abolished ATP-induced eNOS phosphorylation and attenuated the calcium response by the preferential inhibition of CCE. Cholesterol 22-33 nitric oxide synthase 3 Homo sapiens 67-71 28138348-8 2017 Furthermore, cholesterol enrichment also inhibited shear stress-induced NO production and eNOS phosporylation, consistent with our previous results showing a significant role for ATP autocrine stimulation and subsequent activation of CCE in the endothelial flow response. Cholesterol 13-24 nitric oxide synthase 3 Homo sapiens 90-94 29372262-8 2018 The increased cholesterol and triglyceride level and decreased protective HDL level, decreases the activity and expression of eNOS and disrupts the integrity of vascular endothelium, due to oxidative stress. Cholesterol 14-25 nitric oxide synthase 3 Homo sapiens 126-130 26409042-1 2015 Caveolin-1 (Cav-1), the homo-oligomeric coat protein of cholesterol-rich caveolae signalosomes, regulates signaling proteins including endothelial nitric oxide synthase (eNOS). Cholesterol 56-67 nitric oxide synthase 3 Homo sapiens 135-168 25557764-8 2015 Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase. Cholesterol 119-130 nitric oxide synthase 3 Homo sapiens 45-49 24996290-3 2014 Statins are potent modulators of CYP3A4 2 enzyme and endothelial nitric oxide synthase (eNOS) functions in a number of cholesterol-independent, cardio protective actions in T2D. Cholesterol 119-130 nitric oxide synthase 3 Homo sapiens 53-86 24996290-3 2014 Statins are potent modulators of CYP3A4 2 enzyme and endothelial nitric oxide synthase (eNOS) functions in a number of cholesterol-independent, cardio protective actions in T2D. Cholesterol 119-130 nitric oxide synthase 3 Homo sapiens 88-92 22063270-5 2012 Increases in cholesterol levels inversely correlated with neutral sphingomyelinase 2 (NSMase2) activity, endothelial nitric oxide synthase (eNOS) phospho-activation and NO-production. Cholesterol 13-24 nitric oxide synthase 3 Homo sapiens 105-138 23269619-6 2013 Hypertension, diabetes, smoking, total cholesterol, triglycerides, LDLc, HDLc and TT genotype of the eNOS gene were independent risk factors for the development of PCAD. Cholesterol 39-50 nitric oxide synthase 3 Homo sapiens 101-105 23517789-6 2013 CONCLUSIONS: Our results support the idea that, the eNOS E298D polymorphism, which is not associated with hypertension, may increase the risk of hypertension when associated with high serum total-cholesterol levels. Cholesterol 196-207 nitric oxide synthase 3 Homo sapiens 52-56 24577926-3 2014 Single nucleotide polymorphism (SNP) (Glu 298 Asp) in ecNOS was determined in 280 subjects, from Southern Punjab (in Pakistan) population, including (160 ACS patients and 120 healthy controls) by PCR-RFLP method and genotype was correlated with various risk factors as well as with serum cholesterol and triglyceride levels. Cholesterol 288-299 nitric oxide synthase 3 Homo sapiens 54-59 21956531-8 2011 Women without eNOS gene polymorphism at position -786T>C and Intron 4b/a showed a greater reduction of plasma cholesterol levels in response to ET. Cholesterol 113-124 nitric oxide synthase 3 Homo sapiens 14-18 18550157-1 2008 OBJECTIVE: To assess whether the Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene possibly mediates the relation of blood pressure and serum cholesterol. Cholesterol 168-179 nitric oxide synthase 3 Homo sapiens 63-96 18550157-1 2008 OBJECTIVE: To assess whether the Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene possibly mediates the relation of blood pressure and serum cholesterol. Cholesterol 168-179 nitric oxide synthase 3 Homo sapiens 98-102 18550157-4 2008 After adjustment for age, sex, BMI, and lifestyle (drinking, smoking, exercise and stress), the odds ratio (OR) of hypertension associated with high (> or = 220 mg/dl or under treatment) total cholesterol was 2.08 (95% Confidence Interval (CI) 1.02-4.24) among carriers of the eNOS 298Asp allele versus 1.18 (95% CI 0.89-1.55, p for interaction=0.50) among non-carriers. Cholesterol 196-207 nitric oxide synthase 3 Homo sapiens 280-284 18230825-6 2008 The Asp298 allele carriers of the eNOS gene presented significantly higher plasma low density lipoprotein (LDL) cholesterol, LDL particle size, malondialdehyde-modified LDL (MDA-LDL), and fasting insulin levels and lower plasma high density lipoprotein (HDL) cholesterol, apolipoprotein A-I levels, and endothelium-dependent vasodilation when compared with noncarriers. Cholesterol 112-123 nitric oxide synthase 3 Homo sapiens 34-38 18230825-6 2008 The Asp298 allele carriers of the eNOS gene presented significantly higher plasma low density lipoprotein (LDL) cholesterol, LDL particle size, malondialdehyde-modified LDL (MDA-LDL), and fasting insulin levels and lower plasma high density lipoprotein (HDL) cholesterol, apolipoprotein A-I levels, and endothelium-dependent vasodilation when compared with noncarriers. Cholesterol 259-270 nitric oxide synthase 3 Homo sapiens 34-38 16814758-3 2006 Here, we reasoned that since the endothelial nitric oxide synthase is, in part, expressed in cholesterol-rich plasmalemmal microdomains (e.g., caveolae and rafts), amlodipine could interfere with this specific locale of the enzyme and thereby modulate NO production in endothelial cells. Cholesterol 93-104 nitric oxide synthase 3 Homo sapiens 33-66 17110473-8 2007 CONCLUSIONS: Our results suggest that genetic variation at the eNOS locus is associated with features of metabolic syndrome, and might represent a new genetic susceptibility component for insulin resistance, hypertriglyceridemia, and low HDL-cholesterol concentrations. Cholesterol 242-253 nitric oxide synthase 3 Homo sapiens 63-67 17126309-9 2007 NOS3 intron 4A/B STR was associated with increased concentrations of total cholesterol and apo B. Cholesterol 75-86 nitric oxide synthase 3 Homo sapiens 0-4 17126309-12 2007 NOS3 is also related to hypertension, endothelial dysfunction and variation on serum cholesterol in young adults with AMI. Cholesterol 85-96 nitric oxide synthase 3 Homo sapiens 0-4 15916766-0 2006 Endothelial nitric oxide synthase gene variant modulates the relationship between serum cholesterol levels and blood pressure in the general population: new evidence for a direct effect of lipids in arterial blood pressure. Cholesterol 88-99 nitric oxide synthase 3 Homo sapiens 0-33 11986889-5 2002 These effects are reversed, or at least reduced, by lipid-lowering agents and (because LDL cholesterol down-regulates endothelial nitric oxide synthase) by the administration of L-arginine, the substrate for nitric oxide (NO) formation. Cholesterol 91-102 nitric oxide synthase 3 Homo sapiens 118-151 11707586-2 2001 Here we show that in cells lacking caveolae, the dually acylated protein, endothelial nitric oxide synthase (eNOS), localizes to cholesterol-rich lipid raft domains of the plasma membrane. Cholesterol 129-140 nitric oxide synthase 3 Homo sapiens 74-107 11707586-2 2001 Here we show that in cells lacking caveolae, the dually acylated protein, endothelial nitric oxide synthase (eNOS), localizes to cholesterol-rich lipid raft domains of the plasma membrane. Cholesterol 129-140 nitric oxide synthase 3 Homo sapiens 109-113 11673056-2 2001 Recent studies demonstrate that endothelial nitric oxide synthase (eNOS), caveolin, hetero-trimeric G-protein coupled receptors, and a calcium channel form an activation complex that is associated with cholesterol-rich caveolae. Cholesterol 202-213 nitric oxide synthase 3 Homo sapiens 32-65 11350569-15 2001 However, male diabetic patients with eNOS Asp298Asp genotype had higher plasma very-low density lipoprotein (VLDL) cholesterol and VLDL-triglyceride concentrations than those with the genotypes Glu298Glu or Glu298Asp (P < 0.01 for trend). Cholesterol 115-126 nitric oxide synthase 3 Homo sapiens 37-41 11348878-2 2001 Here, we show that simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, within the therapeutic range (0.01 to 1 micromol/L) prevented the downregulation of eNOS mRNA and protein promoted by nLDL (180 mg cholesterol/dL, 48 hours) in human umbilical vein endothelial cells. Cholesterol 224-235 nitric oxide synthase 3 Homo sapiens 177-181 32564765-0 2021 The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy. Cholesterol 83-94 nitric oxide synthase 3 Homo sapiens 17-50 11136695-2 2001 Increased uptake of cholesterol by endothelial cells (ECs) upregulates the abundance of the structural protein caveolin-1 and impairs NO release through the stabilization of the inhibitory heterocomplex between caveolin-1 and endothelial NO synthase (eNOS). Cholesterol 20-31 nitric oxide synthase 3 Homo sapiens 226-249 11136695-2 2001 Increased uptake of cholesterol by endothelial cells (ECs) upregulates the abundance of the structural protein caveolin-1 and impairs NO release through the stabilization of the inhibitory heterocomplex between caveolin-1 and endothelial NO synthase (eNOS). Cholesterol 20-31 nitric oxide synthase 3 Homo sapiens 251-255 10542298-11 1999 We conclude that oxLDL-induced depletion of caveola cholesterol causes eNOS to leave caveolae and inhibits acetylcholine-induced activation of the enzyme. Cholesterol 52-63 nitric oxide synthase 3 Homo sapiens 71-75 10568338-2 1999 Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes. Cholesterol 123-134 nitric oxide synthase 3 Homo sapiens 55-88 10568338-2 1999 Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes. Cholesterol 123-134 nitric oxide synthase 3 Homo sapiens 90-94 10568338-2 1999 Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes. Cholesterol 123-134 nitric oxide synthase 3 Homo sapiens 238-242 32564765-0 2021 The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy. Cholesterol 83-94 nitric oxide synthase 3 Homo sapiens 52-56 32564765-10 2021 However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05). Cholesterol 129-140 nitric oxide synthase 3 Homo sapiens 23-27