関: eNOS

WordNet

any compound of oxygen with another element or a radical
of or relating to or located in the endothelium

PrepTutorEJDIC

《所有・所属》…『の』,…のものである,…に属する・《材料・要素》…『でできた』,から成る・《部分》…『の』[『中の』] ・《数量・単位・種類を表す名詞に付いて》…の・《原因・動機》…『で』,のために(because of) ・《主格関係》…『の』,による,によって・《目的格関係》…『を』,の・《同格関係》…『という』・《関係・関連》…『についての』[『の』],の点で・《抽象名詞などと共に》…の[性質をもつ] ・《『It is』+『形』+『of』+『名』+『to』 doの形で,ofの後の名詞を意味上の主語として》・《分離》…『から』・《起原・出所》…『から』[『の』](out of) ・《『名』+『of』+『a』(『an』)+『名』の形で》…のような・《『名』+『of』+『mine』(『yours, his』など独立所有格)の形で》…の…・《時》(1)《副詞句を作って》…に《形容詞句を作って》…の・《時刻》《米》…前(to,《米》before)
酸化物
窒素の,窒素を含む

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1. Exhaled nitric oxide analysis and applications
2. 重症疾患に関連する神経筋脱力 neuromuscular weakness related to critical illness
3. 一酸化窒素と腎臓 nitric oxide and the kidney
4. 単純ヘルペス性角膜炎 herpes simplex keratitis
5. 心不全における一酸化窒素、その他のホルモン、サイトカイン、およびケモカイン nitric oxide other hormones cytokines and chemokines in heart failure

English Journal

A novel truncated form of eNOS associates with altered vascular function.

Galluccio E1, Cassina L, Russo I, Gelmini F, Setola E, Rampoldi L, Citterio L, Rossodivita A, Kamami M, Colombo A, Alfieri O, Carini M, Bosi E, Trovati M, Piatti P, Monti LD, Casari G.Author information 1Cardio-Diabetes and Core Lab, Division of Metabolic and Cardiovascular Science, San Raffaele Scientific Institute, Via Olgettina 60, Milan, Italy.AbstractAIMS: Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene. We previously reported the genetic association between NOS3 rs753482-A>C polymorphism on intron 19 and coronary artery disease (CAD). In the attempt of conferring functional implication to the rs753482-A>C polymorphism, we investigated its influence on transcript maturation.
Cardiovascular research.Cardiovasc Res.2014 Mar 1;101(3):492-502. doi: 10.1093/cvr/cvt267. Epub 2013 Dec 3.
AIMS: Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene. We previously reported the genetic association between NOS3 rs753482-A>C polymorphism on intron 19 and coronary artery disease (CAD). In the attempt of conferr
PMID 24302629

Simplified 2-aminoquinoline-based scaffold for potent and selective neuronal nitric oxide synthase inhibition.

Cinelli MA1, Li H, Chreifi G, Martásek P, Roman LJ, Poulos TL, Silverman RB.Author information 1Departments of Chemistry and Molecular Biosciences, Chemistry of Life Processes Institute, Center for Molecular Innovation and Drug Discovery, Northwestern University , 2145 Sheridan Road, Evanston, Illinois 60208-3113, United States.AbstractSince high levels of nitric oxide (NO) are implicated in neurodegenerative disorders, inhibition of the neuronal isoform of nitric oxide synthase (nNOS) and reduction of NO levels are therapeutically desirable. Nonetheless, many nNOS inhibitors mimic l-arginine and are poorly bioavailable. 2-Aminoquinoline-based scaffolds were designed with the hope that they could (a) mimic aminopyridines as potent, isoform-selective arginine isosteres and (b) possess chemical properties more conducive to oral bioavailability and CNS penetration. A series of these compounds was synthesized and assayed against purified nNOS enzymes, endothelial NOS (eNOS), and inducible NOS (iNOS). Several compounds built on a 7-substituted 2-aminoquinoline core are potent and isoform-selective; X-ray crystallography indicates that aminoquinolines exert inhibitory effects by mimicking substrate interactions with the conserved active site glutamate residue. The most potent and selective compounds, 7 and 15, were tested in a Caco-2 assay and showed good permeability and low efflux, suggesting high potential for oral bioavailability.
Journal of medicinal chemistry.J Med Chem.2014 Feb 27;57(4):1513-30. doi: 10.1021/jm401838x. Epub 2014 Feb 10.
Since high levels of nitric oxide (NO) are implicated in neurodegenerative disorders, inhibition of the neuronal isoform of nitric oxide synthase (nNOS) and reduction of NO levels are therapeutically desirable. Nonetheless, many nNOS inhibitors mimic l-arginine and are poorly bioavailable. 2-Aminoqu
PMID 24472039

Nogo-B Receptor Modulates Angiogenesis Response of Pulmonary Artery Endothelial Cells Through eNOS Coupling.

Teng RJ1, Rana U, Afolayan AJ, Zhao B, Miao QR, Konduri GG.Author information 1Medical College of Wisconsin, Pediatrics, Children's Research Institute, and Cardiovascular Center, Milwaukee, Wisconsin, United States ; rteng@mcw.edu.AbstractNogo-B, a Reticulon-4 (RTN4) isoform, modulates the motility and adhesion of vascular endothelial cells after binding to its receptor, NgBR. Nogo-B/NgBR pathway contributes to vascular remodeling and angiogenesis, but the role of this pathway in the angiogenesis of developing lungs remains unknown. We previously reported that angiogenesis function of pulmonary artery endothelial cells (PAEC) is impaired by increased reactive oxygen species (ROS) formation in a fetal lamb model of intrauterine pulmonary hypertension (IPH). Here, we report that Nogo-B/NgBR pathway is altered in IPH and that decreased NgBR expression contributes to impaired angiogenesis in IPH. We observed a decrease in NgBR expression in lysates of whole lung or pulmonary artery endothelial cells (PAEC) from fetal lambs with IPH compared to controls. Overexpression of NgBR in IPH PAEC rescued the in vitro angiogenesis defects and increased the phosphorylation of both Akt and endothelial nitric oxide synthase at serine1179 and the expression of both manganese superoxide dismutase and GTP cyclohydrolase-1. Consistent with the phenotype of IPH PAEC, knockdown of NgBR in control PAEC decreased the levels of nitric oxide, increased the levels of reactive oxygen species, and impaired in vitro angiogenesis. Our data demonstrate that NgBR mediates PAEC angiogenesis response through the modulation of Akt/eNOS functions, and its decreased expression is mechanistically linked to IPH related angiogenesis defects in the developing lungs.
American journal of respiratory cell and molecular biology.Am J Respir Cell Mol Biol.2014 Feb 25. [Epub ahead of print]
Nogo-B, a Reticulon-4 (RTN4) isoform, modulates the motility and adhesion of vascular endothelial cells after binding to its receptor, NgBR. Nogo-B/NgBR pathway contributes to vascular remodeling and angiogenesis, but the role of this pathway in the angiogenesis of developing lungs remains unknown.
PMID 24568601

Japanese Journal

NO合成酵素完全欠損マウスの開発

筒井正人,下川宏明,守下敢 [他],中田靖,佐羽内研,中島康秀,柳原延章
藥學雜誌 127(9), 1347-1355, 2007-09-01
… The nitric oxide (NO) synthases (NOSs) system consists of three different isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial NOSs (eNOS). … The roles of NO in vivo have been extensively investigated in pharmacological studies with NOS inhibitors and in studies with mice lacking each NOS isoform. …
NAID 110006380720

Truncated estrogen receptor alpha 46-kDa isoform in human endothelial cells : relationship to acute activation of nitric oxide synthase

FIGTREE GA
Circulation 107, 120-126, 2003
NAID 30022668016

下鼻甲介粘膜擦過細胞のNOS isoform発現に対するIFN-γ,TNF-αの影響

川本浩子,竹野幸夫,夜陣紘治
日本耳鼻咽喉科學會會報 105(2), 158-165, 2002-02-20
… Background: Interest in the physiological, pathological and therapeutic implications of nitric oxide (NO) have grown exponentially, with human nasal cavity and paranasal sinuses considered a dominant source of NO, indicating that this molecule possesses the diversity of biological effects in the regulation of airway clearance and nonspecific cellular immunity. …
NAID 10008382461