PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15166218-0 2004 Three different oxygen-induced radical species in endothelial nitric-oxide synthase oxygenase domain under regulation by L-arginine and tetrahydrobiopterin. Oxygen 16-22 nitric oxide synthase 3 Homo sapiens 50-83 12756290-1 2003 The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline. Oxygen 90-96 nitric oxide synthase 3 Homo sapiens 11-44 15004019-0 2004 Evidence of two distinct oxygen complexes of reduced endothelial nitric oxide synthase. Oxygen 25-31 nitric oxide synthase 3 Homo sapiens 53-86 15004019-1 2004 Oxygen binding to the oxygenase domain of reduced endothelial nitric oxide synthase (eNOS) results in two distinct species differing in their Soret and visible absorbance maxima and in their capacity to exchange oxygen by CO. Oxygen 0-6 nitric oxide synthase 3 Homo sapiens 50-83 15004019-1 2004 Oxygen binding to the oxygenase domain of reduced endothelial nitric oxide synthase (eNOS) results in two distinct species differing in their Soret and visible absorbance maxima and in their capacity to exchange oxygen by CO. Oxygen 22-28 nitric oxide synthase 3 Homo sapiens 50-83 14581231-1 2003 The kinetics of formation and transformation of oxygen complexes of two heme-thiolate proteins (the F393H mutant of cytochrome P450 BM3 and the oxygenase domain of endothelial nitric oxide synthase, eNOS) were studied under high pressure. Oxygen 48-54 nitric oxide synthase 3 Homo sapiens 164-197 12756290-1 2003 The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline. Oxygen 90-96 nitric oxide synthase 3 Homo sapiens 46-50 34547902-14 2021 CMA of SG-eNOS terminates O2 - generation preventing further tissue damage but causes irreversible loss of eNOS and NO availability. Oxygen 26-28 nitric oxide synthase 3 Homo sapiens 10-14 12480940-8 2003 Ferrous eNOS(ox), in the presence of l-arginine, is fully functional in forming the tetrahydrobiopterin radical upon mixing with oxygen as demonstrated by rapid-freeze EPR measurements. Oxygen 129-135 nitric oxide synthase 3 Homo sapiens 8-12 8928825-4 1996 eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation. Oxygen 55-61 nitric oxide synthase 3 Homo sapiens 0-4 8928825-5 1996 In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension. Oxygen 27-33 nitric oxide synthase 3 Homo sapiens 37-41 8928825-6 1996 The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity. Oxygen 4-10 nitric oxide synthase 3 Homo sapiens 31-35 8928825-8 1996 Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability. Oxygen 64-70 nitric oxide synthase 3 Homo sapiens 5-9 8746197-2 1995 The objective of this study was to test the hypothesis that constitutive nitric oxide synthase (cNOS) is sensitive to oxygen tension and that hypoxia increases the activity of cNOS and nitric oxide production in the porcine coronary microcirculation. Oxygen 118-124 nitric oxide synthase 3 Homo sapiens 96-100 8746197-13 1995 CONCLUSIONS: These experiments demonstrated that the regulation of cNOS is sensitive to oxygen tension. Oxygen 88-94 nitric oxide synthase 3 Homo sapiens 67-71 34237174-2 2021 Increased arginase 1 activity leads to reduced nitric oxide (NO) production and increased formation of reactive oxygen species due to uncoupling of the NO-producing enzyme endothelial NO synthase (eNOS). Oxygen 112-118 nitric oxide synthase 3 Homo sapiens 197-201 11779139-4 2002 On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level. Oxygen 124-130 nitric oxide synthase 3 Homo sapiens 48-81 11593517-1 1999 OBJECTIVE: To observe the effects of nerve growth factor (NGF) on nitric oxide (NO) release and constitutive nitric oxide synthase (cNOS) gene expression in oxygen/glucose deprived cortical neuron cultures. Oxygen 157-163 nitric oxide synthase 3 Homo sapiens 132-136 9859864-6 1998 Compared to controls, the amount of eNOS transcripts was found to be elevated at low-oxygen tension, however, cNOS protein was downregulated after 24 h in the hypoxic environment, as shown by immunocytochemistry and Western blot analysis. Oxygen 85-91 nitric oxide synthase 3 Homo sapiens 36-40 8655601-6 1996 Cobalt inhibited the expression of cNOS transcripts, suggesting a mechanism comparable to that by which oxygen tension regulates expression of other vasoregulatory genes. Oxygen 104-110 nitric oxide synthase 3 Homo sapiens 35-39 35332670-0 2022 Intelligent Nanodelivery System-Generated 1 O2 Mediates Tumor Vessel Normalization by Activating Endothelial TRPV4-eNOS Signaling. Oxygen 44-46 nitric oxide synthase 3 Homo sapiens 115-119 34502464-3 2021 Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma. Oxygen 82-85 nitric oxide synthase 3 Homo sapiens 14-47 34502464-3 2021 Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma. Oxygen 82-85 nitric oxide synthase 3 Homo sapiens 49-53 34502464-6 2021 Both treatment with L-sepiapterin and eNOS downregulation induced increased nitric oxide (NO) and decreased O2 levels, triggering NOS coupling and reducing cell growth and resistance to anoikis and dacarbazine chemotherapy. Oxygen 108-110 nitric oxide synthase 3 Homo sapiens 38-42 33548859-7 2021 The uncoupling of eNOS triggers a switch of its activity from a NO-producing enzyme to a NADPH oxidase-like system generating O2 -, thereby potentiating ROS production and oxidative stress. Oxygen 126-130 nitric oxide synthase 3 Homo sapiens 18-22 33140223-1 2021 Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function. Oxygen 347-353 nitric oxide synthase 3 Homo sapiens 226-230 33140223-1 2021 Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function. Oxygen 347-353 nitric oxide synthase 3 Homo sapiens 243-247 30641122-17 2019 The presence of a minor allele in G894T polymorphism of the NOS3 gene contributes to formation of oxygen transport function of blood. Oxygen 98-104 nitric oxide synthase 3 Homo sapiens 60-64 32122268-7 2021 Stem cell/oxygen-releasing HP system increased cGMP level and nNOS, eNOS, a-SMA and M3 expression, while decreasing fibrosis and apoptosis in the corpus cavernosum. Oxygen 10-16 nitric oxide synthase 3 Homo sapiens 68-72 31914408-1 2020 Production of reactive oxygen species due to dysregulated endothelial nitric oxide synthase (eNOS) activity is linked to vascular dysfunction. Oxygen 23-29 nitric oxide synthase 3 Homo sapiens 58-91 31920721-9 2019 In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1). Oxygen 45-51 nitric oxide synthase 3 Homo sapiens 126-159 30135282-9 2018 The data obtained suggest that if the oxygen supply of the organism is impaired, the endothelial nitric oxide synthase G894T polymorphism may be important for the oxidative stress development. Oxygen 38-44 nitric oxide synthase 3 Homo sapiens 85-118 28395329-9 2017 We found that under lowered oxygen condition, 1,25(OH)2D3 could upregulate EC eNOS, p-eNOSSer1177, and p-AktSer473 expression, but inhibit cleaved ROCK1 expression. Oxygen 28-34 nitric oxide synthase 3 Homo sapiens 78-82 29466710-1 2018 Uncoupled endothelial nitric oxide synthase (eNOS) produces O2- instead of nitric oxide (NO). Oxygen 60-62 nitric oxide synthase 3 Homo sapiens 10-43 29466710-1 2018 Uncoupled endothelial nitric oxide synthase (eNOS) produces O2- instead of nitric oxide (NO). Oxygen 60-62 nitric oxide synthase 3 Homo sapiens 45-49 28803324-2 2017 NO is a gas synthesized from Larginine (a conditionally essential amino acid) and oxygen by endothelial nitric oxide synthase (eNOS). Oxygen 82-88 nitric oxide synthase 3 Homo sapiens 92-125 24096875-0 2013 p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation. Oxygen 46-52 nitric oxide synthase 3 Homo sapiens 102-106 26019598-7 2014 eNOS is a subgroup of this family of enzymes that catalyses the production of nitric oxide (NO) from L-arginine and oxygen, which leads to vascular relaxation by activating the guanylate cyclase. Oxygen 116-122 nitric oxide synthase 3 Homo sapiens 0-4 24755153-1 2014 BACKGROUND: Glutathionylation of endothelial nitric oxide synthase (eNOS) "uncouples" the enzyme, switching its function from nitric oxide (NO) to O2( -) generation. Oxygen 147-149 nitric oxide synthase 3 Homo sapiens 33-66 26823875-10 2015 Interactions were existed between NOS3 gene polymorphisms and oxygen therapy duration. Oxygen 62-68 nitric oxide synthase 3 Homo sapiens 34-38 26416428-9 2015 Levels of phosphorylated Akt, anti-apoptotic Bcl-xL, pro-apoptotic Bax and endothelial nitric oxide synthase (NOS) were re-regulated after combined oxygen and melatonin delivery, whereas neuronal and inducible NOS, which were increased by oxygen treatment, were not influenced by melatonin. Oxygen 148-154 nitric oxide synthase 3 Homo sapiens 75-108 26286023-1 2015 Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease. Oxygen 94-100 nitric oxide synthase 3 Homo sapiens 0-33 26286023-1 2015 Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease. Oxygen 94-100 nitric oxide synthase 3 Homo sapiens 35-39 24096875-4 2013 p53 exhibited a differential DNA-binding, namely, BAX-p53RE in the infarct heart or NOS3-p53RE in the oxygenated heart, which was regulated by oxygen-induced, post-translational modification of p53. Oxygen 102-108 nitric oxide synthase 3 Homo sapiens 84-88 22929836-9 2012 Under oxidative stress conditions, eNOS for example can switch from producing NO to O2 - in a process called uncoupling, which is believed to be caused by oxidation of heme or the co-factor, tetrahydrobiopterin (BH4). Oxygen 84-86 nitric oxide synthase 3 Homo sapiens 35-39 23977830-1 2013 S-Glutathionylation is a redox-regulated modification that uncouples endothelial nitric oxide synthase (eNOS), switching its function from nitric oxide (NO) synthesis to ( )O2(-) generation, and serves to regulate vascular function. Oxygen 173-175 nitric oxide synthase 3 Homo sapiens 104-108 23395155-5 2013 In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide-producing enzyme. Oxygen 19-25 nitric oxide synthase 3 Homo sapiens 84-88 23122309-8 2012 NOS3 gene plays a role in regulating vascular tone and blood vessel diameter, which may be altered by the low-oxygen environment of Tibet. Oxygen 110-116 nitric oxide synthase 3 Homo sapiens 0-4 17698846-4 2007 In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (>90%), and the measured stoichiometry of O(2)/NADPH is very close to the theoretical value. Oxygen 128-132 nitric oxide synthase 3 Homo sapiens 60-64 21638020-11 2012 In conclusion, this study demonstrated that dietary Arg or NCG supplementation may affect microRNAs (miR-15b, miR-222) targeting VEGFA and eNOS gene expressions in umbilical vein, so as to regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue for fetal development and survival, and enhance the reproductive performance of sows. Oxygen 272-278 nitric oxide synthase 3 Homo sapiens 139-143 21179168-2 2010 In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. Oxygen 206-212 nitric oxide synthase 3 Homo sapiens 38-42 20213497-5 2010 Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Oxygen 251-257 nitric oxide synthase 3 Homo sapiens 74-78 17698846-5 2007 We report for the first time that the presence of L-arginine stimulates oxygen uptake by eNOS. Oxygen 72-78 nitric oxide synthase 3 Homo sapiens 89-93 17698846-8 2007 These results reveal different mechanisms for oxygen metabolism for eNOS as opposed to nNOS and, perhaps, partially explain their functional differences. Oxygen 46-52 nitric oxide synthase 3 Homo sapiens 68-72 16997880-1 2006 We determined the effect of oxygen [approximately 100 Torr (normoxia) and approximately 30-40 Torr (hypoxia)] on functions of endothelial nitric oxide (NO) synthase (NOS-3) and its negative regulator caveolin-1 in ovine fetal and neonatal lung microvascular endothelial cells (MVECs). Oxygen 28-34 nitric oxide synthase 3 Homo sapiens 166-171 17486142-6 2007 Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation. Oxygen 55-61 nitric oxide synthase 3 Homo sapiens 14-18 17486142-6 2007 Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation. Oxygen 55-61 nitric oxide synthase 3 Homo sapiens 87-91 16997880-9 2006 These data support our hypothesis that increased Po(2) at birth promotes dissociation of caveolin-1 and NOS-3, with an increase in their activities, and that PKC and an oxygen-sensitive cell surface G protein-coupled receptor regulate caveolin-1 and NOS-3 interactions in fetal and neonatal lung MVECs. Oxygen 169-175 nitric oxide synthase 3 Homo sapiens 250-255 16689381-3 2006 In addition, ischemia will also be controlled by decreasing oxygen demand related to BP and HR, and with increasing oxygen supply by increased ECNOS gene expression, collateral formation and regression of coronary stenosis. Oxygen 116-122 nitric oxide synthase 3 Homo sapiens 143-148