ライフサイエンスコーパス: endothelial NOS

1 on and stimulates EC migration by activating endothelial NOS (eNOS).

2 m drives OxLDL-mediated arginase activation, endothelial NOS uncoupling, endothelial dysfunction, and

3 ation of antisense constructs did not affect endothelial NOS, as evidenced by a spared NO release aft

4 of Cys-298 to sulfenic acid via the PI3K/Akt/endothelial NOS pathway.

5 Although endothelial NOS responses are depressed in congestive he

6 rther demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-(3)H-arginine to

7 ive nitric oxide synthase (NOS) activity and endothelial NOS protein abundance.

8 Total NOS activity and endothelial NOS protein levels were unchanged.

9 tions; total NO synthase (NOS) activity; and endothelial NOS protein levels.

10 and involve persistent activation of Akt and endothelial NOS (eNOS), as well as activity of the downs

11 in phosphorylation and activation of AKT and endothelial NOS.

12 resulted in phosphorylation of both Akt and endothelial NOS.

13 ng1/Tie2, phosphoinositide 3-kinase/Akt, and endothelial NOS pathways appear to mediate Niacin-induce

14 ascular endothelial growth factor, Ang1, and endothelial NOS expression in cultured astrocytes, and d

15 al nitric-oxide synthase (nNOS or NOS I) and endothelial NOS (eNOS or NOS III) differ widely in their

16 istinct catalytic behaviors of inducible and endothelial NOS (iNOS and eNOS).

17 crystallographic structures of inducible and endothelial NOS oxygenase domains cocrystallized with ch

18 ate a role for mechanical stress in iNOS and endothelial NOS (eNOS) regulation.

19 f inducible nitric-oxide synthase (iNOS) and endothelial NOS (eNOS) and the expression of heat shock

20 protein content of inducible NOS (iNOS) and endothelial NOS (eNOS) in the myocytes.

21 f inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) on the acute inflammatory respons

22 f inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) on the renal effects of lipopolys

23 orms neuronal NOS, inducible NOS (iNOS), and endothelial NOS in a protein kinase A-dependent manner.

24 pha, direct ERalpha-Galphai interaction, and endothelial NOS (eNOS) activation.

25 hyl ester on inducible NOS (macrophages) and endothelial NOS in vitro (aorta) and in vivo (blood pres

26 To determine whether neuronal NOS (nNOS) and endothelial NOS (eNOS) are critical in excitotoxic damag

27 article reviews how neuronal NOS (nNOS) and endothelial NOS (eNOS) knockout mice have contributed to

28 sidue C termini from neuronal NOS (nNOS) and endothelial NOS (eNOS), respectively.

29 f wild-type (Wt) and neuronal NOS (nNOS) and endothelial NOS (eNOS)-deficient mice.

30 on recombinant human neuronal NOS (nNOS) and endothelial NOS (eNOS).

31 nNOS- and endothelial NOS-deficient mice maintain erectile functio

32 ntrast, inhibition of human neuronal NOS and endothelial NOS (eNOS) was relatively weaker, rapidly re

33 t interact with and inhibit neuronal NOS and endothelial NOS, macrophage proteins that inhibit NOS2 h

34 itric-oxide synthase [NOS; inducible NOS and endothelial NOS], and cyclooxygenase (COX-2) in the LP e

35 n be formed by both neuronal NO synthase and endothelial NOS (eNOS).

36 -PCR revealed that inducible NO synthase and endothelial NOS but not neuronal NOS genes were expresse

37 ived macrophages (BMDMOs) from wild-type and endothelial NOS (eNOS) knock-out (KO) mice have been use

38 three NOS isoforms, neuronal, inducible, and endothelial NOSs, in 2D and 3D cultures.

39 using anti-neuronal NOS (nNOS), but not anti-endothelial NOS (eNOS) or anti-inducible NOS (iNOS) anti

40 protein expression was further enhanced, but endothelial NOS phosphorylation was reduced in cardiac t

41 cited by acetylcholine (ACh) and mediated by endothelial NOS dilator.

42 ance between NO and superoxide production by endothelial NOS (eNOS coupling).

43 icantly increased by nNOS, but unaffected by endothelial NOS or inducible NOS.

44 ILK deletion caused endothelial NOS (eNOS) uncoupling, reflected in reduced

45 In endothelial cells, endothelial NOS activation per se inhibited LDL oxidatio

46 ardiomyocytes are also deficient in cellular endothelial NOS, but overexpress mtNOS, which allowed us

47 own previously that NO from the constitutive endothelial NOS (eNOS) is necessary to obtain maximal iN

48 In contrast, endothelial NOS protein content and calcium-dependent NO

49 We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl rad

50 activation of the Ca2+-calmodulin-dependent endothelial NOS (eNOS).

51 -(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor].

52 with targeted deletion of the gene encoding endothelial NOS (eNOS(-/-)) display dramatic reductions

53 antly, the selectivities for nNOS over eNOS (endothelial NOS), and iNOS (inducible NOS) are greatly i

54 d and assayed against purified nNOS enzymes, endothelial NOS (eNOS), and inducible NOS (iNOS).

55 For example, endothelial NOS controls blood pressure, blood flow and

56 re that motor neurons constitutively express endothelial NOS that helps support the survival of motor

57 but the role of the constitutively expressed endothelial NOS (eNOS) is unclear.

58 induced radical intermediates in the ferrous endothelial NOS oxygenase domain (eNOSox) with or withou

59 mozygous targeted disruption of the gene for endothelial NOS (eNOS) were studied in an experimental m

60 constitutive NOS in vitro, in particular for endothelial NOS (eNOS).

61 ogical (Nomega-nitro-L-arginine) or genetic (endothelial NOS or inducible NOS) inhibition of NOSs in

62 Heat shock was found to enhance Hsp90/endothelial NOS interactions and produce higher NO.

63 ults strongly indicate that Glu-361 in human endothelial NOS is specifically involved in the interact

64 We have altered Glu-361 in human endothelial NOS to Gln or Leu by site-directed mutagenes

65 ly 7.9.10(-5) m, respectively, whereas human endothelial NOS was hardly affected at all.

66 olated vessels, and whole animals identified endothelial NOS activation as a fundamental requirement

67 ntified early protein oxidation and impaired endothelial NOS homodimer formation as plausible mechani

68 itivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes com

69 lot analysis revealed a 1.9-fold increase in endothelial NOS protein and a 37% decrease in DDAH I pro

70 o normal in mice with a targeted mutation in endothelial NOS (eNOS-), but LTP in stratum radiatum of

71 or deletions in the corresponding region in endothelial NOS modestly increase activity under some co

72 3-K)/Akt pathway, which is known to increase endothelial NOS (eNOS) activity by direct phosphorylatio

73 Increased endothelial NOS levels correlated with alterations in ga

74 Instead, we identified increased endothelial NOS s-glutathionylation as the main mechanis

75 o normal C57BL/6J mice resulted in increased endothelial NOS (eNOS) protein levels and NO production

76 uples endothelial NOS activity and increases endothelial NOS-dependent O(2)() production.

77 and P67phox), Mn SOD, inducible NOS (iNOS), endothelial NOS (eNOS), and nitrotyrosine were elevated

78 er two nitric oxide synthase (NOS) isoforms (endothelial NOS and inducible NOS).

79 e for synthesis of NO, exists in 3 isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducib

80 responsible using transgenic animals lacking endothelial NOS (ecNOS).

81 ed the role of the 3 isoforms of NOS, namely endothelial NOS (eNOS), neuronal NOS (nNOS), and inducib

82 retina, neuronal NOS-deficient [nNOS(-/-)], endothelial NOS-deficient [eNOS(-/ -)], and immunologic

83 ists in three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS).

84 ynthase (NOS) isoforms: neuronal NOS (nNOS), endothelial NOS, and immunologic NOS (iNOS).

85 ynthesized and tested against purified nNOS, endothelial NOS (eNOS), and inducible NOS (iNOS) enzymes

86 mpared with control subjects, inducible NOS, endothelial NOS, and nitrotyrosine, but not neuronal NOS

87 different physiological role: neuronal NOS, endothelial NOS, and inducible NOS (iNOS).

88 minimal expression of inducible NOS (NOS2), endothelial NOS (NOS3), and GTPCH-1 protein and nearly u

89 OS) activity and neuronal NOS (nNOS) but not endothelial NOS (eNOS) phosphorylation in rats.

90 is revealed that neuronal NOS (nNOS) but not endothelial NOS (eNOS) protein expression was higher in

91 suggest that nNOS and inducible NOS but not endothelial NOS are irreversibly inhibited by H2S/NO at

92 Deficiency of NOS1 (but not endothelial NOS, NOS3) leads to profound increases in XO

93 e expression of inducible NOS (iNOS) but not endothelial NOS.

94 expression of neuronal NOS and iNOS but not endothelial NOS.

95 y inhibiting calcium-dependent activation of endothelial NOS (eNOS).

96 Because activity of endothelial NOS (eNOS) is thought to be regulated by its

97 ssues were used for Western blot analysis of endothelial NOS and DDAH I expression, measurement of lu

98 eases zinc from the zinc-thiolate cluster of endothelial NOS (eNOS) and presumably forms disulfide bo

99 rginine to [3H]citrulline and the content of endothelial NOS isoenzyme (eNOS) was compared by Western

100 Deficiency of endothelial NOS (eNOS) suppresses retinal but not choroi

101 al structure of the catalytic heme domain of endothelial NOS complexed with 7-NIBr at 1.65 A resoluti

102 the crystal structure of the heme domain of endothelial NOS in tetrahydrobiopterin (H4B)-free and -b

103 n with ADP-sepharose, revealed expression of endothelial NOS (eNOS or NOS3) in tissues from preterm,

104 Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was una

105 In intracerebral RG2 gliomas, expression of endothelial NOS in the tumor was detected at higher leve

106 Expressions of endothelial NOS (eNOS) and neuronal NOS, but not inducib

107 However, the functional importance of endothelial NOS (eNOS) in the rejecting allografts remai

108 ) inhibitor L-NIO, and genetic inhibition of endothelial NOS, implicating peroxynitrous acid as a key

109 ncreases blood pressure due to inhibition of endothelial NOS, resulting in activation of the arterial

110 des derived from the 45-amino acid insert of endothelial NOS were found to potently inhibit binding o

111 oviral vector, a dominant negative mutant of endothelial NOS (TeNOS) was expressed bilaterally in the

112 rotein oxidation and increased occurrence of endothelial NOS monomers in the aortic grafts already du

113 hether adenoviral-mediated overexpression of endothelial NOS (eNOS) could enhance erectile responses,

114 dependent increase in the phosphorylation of endothelial NOS at Ser-1177 and, even in the absence of

115 nM) and uPA-PAI-1 induced phosphorylation of endothelial NOS-Ser(1177) in PMVECs, which was followed

116 In HC, immuno-reactivity of endothelial NOS was decreased, that of inducible NOS was

117 ay be attributable to the down-regulation of endothelial NOS expression.

118 up-regulation of iNOS and down-regulation of endothelial NOS, neuronal NOS, and VEGF, an effect that

119 ss and acetylcholine-mediated stimulation of endothelial NOS significantly increased venous nitrite l

120 with QT prolongation due to hERG activity or endothelial NOS mediated vasoconstriction effect.

121 osporine-treated wild-type (WT) iNOS(-/-) or endothelial NOS (eNOS)(-/-) recipients.

122 e for either inducible NO synthase (iNOS) or endothelial NOS (eNOS) had been ablated.

123 , mice treated with pan-NO synthase (NOS) or endothelial NOS (eNOS) inhibitors, and mice with null mu

124 The selectivities for nNOS over endothelial NOS and inducible NOS of the most potent nNO

125 NOS as well as high selectivity of nNOS over endothelial NOS was retained in some of these compounds

126 iNOS enzyme that were highly selective over endothelial NOS (eNOS).

127 e potent for neuronal NOS and selective over endothelial NOS compared to their trans-counterparts.

128 The myristoyl protein endothelial NOS (eNOS) is present in the dendrites of CA

129 Pulmonary endothelial NOS levels increased and alveolar vascular s

130 To determine whether the recombinant endothelial NOS (eNOS) gene can be delivered in vivo to

131 reversed hypertrophy and fibrosis, recoupled endothelial NOS, lowered oxidant stress, and improved ch

132 Long-term treatment with vitamin C restored endothelial NOS activity in aortas of apoE-deficient mic

133 /- mice and in mice treated with a selective endothelial NOS (eNOS) inhibitor.

134 Despite their structural similarity, endothelial NOS (eNOS) has a 6-fold lower NO synthesis a

135 y increases in response to Ca(2+)-stimulated endothelial NOS (eNOS) activity, and in aortic rings, en

136 eptors reduces HR in 1CH rats and stimulates endothelial NOS in 1 and 3CH rats to decrease ABP and in

137 Therefore, targeting endothelial NOS in the donor represents a promising stra

138 imilar in isolated myocytes, indicating that endothelial NOS likely explains the age difference.

139 bound to a 20 residue peptide comprising the endothelial NOS (eNOS) CaM-binding region establishes th

140 ve investigated BH(4) redox functions in the endothelial NOS (eNOS).

141 in NADPHd reactivity and an induction of the endothelial NOS (eNOS) isoform in microvessels surroundi

142 nt NOS inhibitors, and the structures of the endothelial NOS heme domain complexed with isothioureas

143 effects of substrate/cofactor binding on the endothelial NOS isoform (eNOS).

144 We hypothesized that the endothelial NOS (eNOS) isoform within the RVLM and CVLM

145 e of larger bisisothioureas complexed to the endothelial NOS heme domain has been determined.

146 tures of the inhibitors bound to nNOS and to endothelial NOS.

147 ical studies, using polyclonal antibodies to endothelial NOS and inducible NOS, revealed a diffuse pa

148 fold higher selectivity for iNOS compared to endothelial NOS (eNOS).

149 t the hsp90 inhibitor geldanamycin uncouples endothelial NOS activity and increases endothelial NOS-d

150 NO, derived from pulmonary vascular endothelial NOS, contributes to intrapulmonary vasodilat

151 Venous endothelial NOS expression was unaffected by clinical de

152 s were >1,000-fold selective for iNOS versus endothelial NOS dimerization in a cell-based assay.

153 te NO in response to agonist stimulation via endothelial NOS (eNOS).

154 vo selectivity for the inhibition of iNOS vs endothelial NOS.

155 reased along neural differentiation, whereas endothelial NOS expression was augmented in conditions o

156 either T(H)1 or T(H)2 cell lineages, whereas endothelial NOS (eNOS) or neuronal NOS (nNOS) mutant mic

157 ever, there is controversy regarding whether endothelial NOS (eNOS) can also produce O-2.

158 It is unknown whether endothelial NOS, neuronal NOS, or both caused the elevat

159 dynamic intravascular NO metabolism in which endothelial NOS-derived NO is stabilized as nitrite, tra

160 Nitration correlated with endothelial NOS-3 expression and not with NOS-2-producin