ライフサイエンスコーパス: S-nitrosoglutathione

1 sensitive to glutathione and its derivative S-nitrosoglutathione.

2 stant to the toxic effect of glutathione and S-nitrosoglutathione.

3 er molecule for nitric oxide, in the form of S-nitrosoglutathione.

4 cts such as S-(hydroxymethyl)glutathione and S-nitrosoglutathione.

5 activity was potentiated by the presence of S-nitrosoglutathione.

6 by the physiologically relevant nitrosothiol S-nitrosoglutathione.

7 lular proteins when the cells are exposed to S-nitrosoglutathione.

8 r GSH concentration is high and NOS can form S-nitrosoglutathione.

9 ely long-lived bioactive forms of NO such as S-nitrosoglutathione.

10 ase (GSNOR), which metabolizes the NO adduct S-nitrosoglutathione.

11 ivation and S-nitrosylation of RyR2 required S-nitrosoglutathione.

12 ier molecule for nitric oxide in the form of S-nitrosoglutathione.

13 Incubation of S-nitrosocysteine or S-nitrosoglutathione (5-100 M) in the presence of a gene

14 Using the transnitrosation agent, S-nitrosoglutathione, a kinetic analysis of the selectiv

15 by S-nitrosylation, preventing scavenging of S-nitrosoglutathione, a major cellular bio-reservoir of

16 xation responses for RBCs were compared with S-nitrosoglutathione across a range of O2 tensions.

17 In contrast, S-nitrosoglutathione activates RyR1 by oxidation and S-n

18 The NO donor S-nitrosoglutathione also induced apoptosis and cell lev

19 xp3 by pharmacological drugs was reversed by S-nitrosoglutathione, an NO donor.

20 ice show decreased GSH/GSSG ratio, increased S-nitrosoglutathione and 3-nitrotyrosine in the intestin

21 t homogenates with the S-nitrosylating agent S-nitrosoglutathione and determined maximal SNO occupanc

22 l stimuli induced by exposure to H(2)O(2) or S-nitrosoglutathione and DNA damage inducers.

23 eactions using a chemical nitric oxide donor S-nitrosoglutathione and enzymatic ADP-ribosyltransferas

24 cation of the killing of Escherichia coli by S-nitrosoglutathione and hydrogen peroxide and of Salmon

25 we quantified the ability of nitrosothiols (S-nitrosoglutathione and S-nitroso-N-acetyl-d,l-penicill

26 al reactions are obtained from photolysis of S-nitrosoglutathione and S-nitroso-N-acetyl-DL-penicilla

27 Moreover, S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine

28 model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine

29 was reversed by arginine, and the NO donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine

30 pha stimulation in the presence of NO donors S-nitrosoglutathione and sodium nitroprusside.

31 for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as such, should be considered

32 times faster than that for its reaction with S-nitrosoglutathione, and consistent with Cys 34 being l

33 usside, S-nitroso-N-acetylpenicillamine, and S-nitrosoglutathione, and H2O2 at concentrations less th

34 hyl) aminodiazen-1-ium-1,2-diolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamin

35 is laboratory has shown that glutathione and S-nitrosoglutathione are directly toxic to mycobacteria.

36 s laboratory have shown that glutathione and S-nitrosoglutathione are directly toxic to mycobacteria.

37 Other nitrosothiols such as S-nitrosoglutathione are not substrates for transport an

38 nd GSSG, S-oxidised glutathione species, and S-nitrosoglutathione as oxidation products with the latt

39 A nitric oxide (NO) donor compound, S-nitrosoglutathione, at concentrations as low as 100 nM

40 Here we report that the NO donors NOC-12 and S-nitrosoglutathione both activate RyR1 by release of NO

41 glutathione, A4V SOD and G37R SOD catalyzed S-nitrosoglutathione breakdown three times more efficien

42 ehyde-3-phosphate dehydrogenase with GSSG or S-nitrosoglutathione, but these glutathionyl donors were

43 However, the NO donor S-nitrosoglutathione caused an acute increased Ca(2+) sp

44 Treatment of rat liver microsomes with S-nitrosoglutathione caused S-nitrosylation of CYP2B pro

45 ensitivity of this strain to glutathione and S-nitrosoglutathione compared to that of the wild-type b

46 S-nitrosoglutathione concentrations were higher in mutan

47 S-Nitrosoglutathione-corrected Delta F508 CFTR exhibited

48 minimally active on CFTR; 3) a novel agent, S-nitrosoglutathione diethyl ester, bypasses the need fo

49 was added to the same mixture, the yield of S-nitrosoglutathione dramatically decreased as the activ

50 ischemia/reperfusion model and antimicrobial S-nitrosoglutathione-driven transnitrosylation of an ent

51 diethylamine NONOate, spermine NONOate, and S-nitrosoglutathione, exhibited concentration-dependent

52 e or with S-nitroso-L-cysteine indicate that S-nitrosoglutathione formation is favored.

53 In contrast, D-S-nitrosocysteine, S-nitrosoglutathione, glyceryl trinitrate, and sodium ni

54 Vehicle (0.9% NaCl), 1 micromol/kg S-nitrosoglutathione (GSNO) (an NO(.) donor), or 3 micro

55 We investigated the mechanisms by which S-nitrosoglutathione (GSNO) alters cystic fibrosis trans

56 The mechanism of interaction between S-nitrosoglutathione (GSNO) and hemoglobin is a crucial

57 SE2472 is also more resistant to S-nitrosoglutathione (GSNO) and hydrogen peroxide (H(2)O

58 The endogenous signaling molecule S-nitrosoglutathione (GSNO) and other S-nitrosylating ag

59 ts of nitric oxide (NO) derivatives, such as S-nitrosoglutathione (GSNO) and peroxynitrite, were inve

60 covery, GA-treated hearts were perfused with S-nitrosoglutathione (GSNO) as a source of *NO.

61 nsor for the detection and quantification of S-nitrosoglutathione (GSNO) as a step toward the determi

62 We report that S-nitrosylation of NPR1 by S-nitrosoglutathione (GSNO) at cysteine-156 facilitates

63 onstrated previously that the degradation of S-nitrosoglutathione (GSNO) by cells absolutely required

64 S-Nitrosoglutathione (GSNO) can be electrocatalytically

65 trosylation occurs in IPC hearts and whether S-nitrosoglutathione (GSNO) elicits similar effects on S

66 In vitro, the formation of S-nitrosoglutathione (GSNO) from .NO and excess glutathi

67 hree compounds that exclude GSNOR substrate, S-nitrosoglutathione (GSNO) from its binding site in GSN

68 of Escherichia coli to the nitrosating agent S-nitrosoglutathione (GSNO) in both aerobic and anaerobi

69 ted to selection by exposure to the NO donor S-nitrosoglutathione (GSNO) in concentrations sufficient

70 that can denitrosylate proteins in vivo and S-nitrosoglutathione (GSNO) in vitro However, a periplas

71 at treatment with the physiological NO donor S-nitrosoglutathione (GSNO) increased the abundance of s

72 cells were subjected to oxygen, peroxide or s-nitrosoglutathione (GSNO) induced stress.

73 S-nitrosoglutathione (GSNO) is a nitric oxide donor that

74 S-nitrosoglutathione (GSNO) is a nitric oxide donor that

75 Incubation of purified AIIt with S-nitrosoglutathione (GSNO) led to the inhibition of AII

76 y, we found that application of the NO donor S-nitrosoglutathione (GSNO) or diethylammonium (Z)-1-1(N

77 d EA.hy926 endothelial cells were exposed to S-nitrosoglutathione (GSNO) or diethylenetriamine NONOat

78 apable of modest activation of proMMP-9, but S-nitrosoglutathione (GSNO) or the NONOates, DEA-NO, SPE

79 re we use a similar approach to confirm that S-nitrosoglutathione (GSNO) primarily impacts the metabo

80 In contrast, the NO-releasing compound S-nitrosoglutathione (GSNO) promoted S-glutathionylation

81 avohemoglobin denitrosylase consumes NO, and S-nitrosoglutathione (GSNO) reductase metabolizes GSNO.

82 e regulators of S-nitrosylation, for example S-nitrosoglutathione (GSNO) reductase, provide for a sup

83 mediator of endogenous bronchoconstriction, S-nitrosoglutathione (GSNO) reductase.

84 S-nitroso-L-cysteine-ethyl ester (SNCEE) and S-nitrosoglutathione (GSNO) that cause intracellular and

85 5) in this issue report on the capability of S-nitrosoglutathione (GSNO) to increase the expression,

86 S-Nitrosoglutathione (GSNO) undergoes spontaneous degrad

87 tion of glutathione (GSH) in the presence of S-nitrosoglutathione (GSNO) was examined as a model reac

88 Glial-derived s-nitrosoglutathione (GSNO) was identified as a potent i

89 tion was S-nitroglutathione (GSNO2) and that S-nitrosoglutathione (GSNO) was not a detectable product

90 aldose reductase (AR) due to modification by S-nitrosoglutathione (GSNO) were investigated.

91 telet production, we exposed Meg-01 cells to S-nitrosoglutathione (GSNO) with or without thrombopoeit

92 S-nitrosoglutathione (GSNO), a naturally occurring const

93 is model, we determined the effectiveness of S-nitrosoglutathione (GSNO), a nitric oxide donor with r

94 In contrast, both SNOmetHb and S-nitrosoglutathione (GSNO), a putative intermediate in

95 S-nitrosoglutathione (GSNO), an endogenous bronchodilato

96 er, the NOC-18 effect could be reproduced by S-nitrosoglutathione (GSNO), an endogenous nitrosonium d

97 we found that endogenous nitric oxide (NO), S-nitrosoglutathione (GSNO), and antioxidants blocked se

98 sion was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidas

99 Further, this activity is mediated by S-nitrosoglutathione (GSNO), and GSNO activation by gamm

100 tudy, we show that S-nitrosocysteine (CSNO), S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenic

101 isiae and mouse macrophages that metabolizes S-nitrosoglutathione (GSNO), and show that it is the glu

102 However, a simultaneous increase in S-nitrosoglutathione (GSNO), another NO source for S-nit

103 es and is inhibited by hydrogen peroxide and S-nitrosoglutathione (GSNO), donors of reactive oxygen a

104 oxide (NO) from endogenous sources, such as S-nitrosoglutathione (GSNO), has significant implication

105 esence of a nitric oxide-producing compound, S-nitrosoglutathione (GSNO), Hcp appears to be the prima

106 The endogenous bronchodilator, S-nitrosoglutathione (GSNO), increases expression, matur

107 )) of the E67L enzyme in reactions involving S-nitrosoglutathione (GSNO), S-hydroxymethylglutathione

108 Here, the NO reactive agents, S-nitrosoglutathione (GSNO), S-nitroso-N-acetyl-dl-penac

109 thiazoline-6-sulfonic acid), when exposed to S-nitrosoglutathione (GSNO), S-nitrosocysteine, or S-nit

110 types were used to assess the involvement of S-nitrosoglutathione (GSNO), the primary NO source, in c

111 milar results were found with the tripeptide S-nitrosoglutathione (GSNO), thought to be a donor of NO

112 treated endothelial cells with an NO donor, S-nitrosoglutathione (GSNO), to determine its effect(s)

113 ive nitrogen intermediates (RNI) nitrite and S-nitrosoglutathione (GSNO), which are bactericidal in v

114 etermine a minimal mechanism for spontaneous S-nitrosoglutathione (GSNO)-mediated transnitrosation of

115 e applying nitrosative stress by addition of S-nitrosoglutathione (GSNO).

116 n product derived from homolytic cleavage of S-nitrosoglutathione (GSNO).

117 NOR1) which turns over the natural NO donor, S-nitrosoglutathione (GSNO).

118 olizes the naturally occurring nitrosothiol, S-nitrosoglutathione (GSNO).

119 everse the apoptosis induced by the NO donor S-nitrosoglutathione (GSNO).

120 ) oxidation associated with the formation of S-nitrosoglutathione (GSNO).

121 ) activity after treatment with the NO donor S-nitrosoglutathione (GSNO).

122 cysteine (SNC, 100 mumol/L or 1 mmol/L), and S-nitrosoglutathione (GSNO, 1 mmol/L).

123 w that hmp expression is also upregulated by S-nitrosoglutathione (GSNO, widely used as an NO release

124 Cardiomyocytes were exposed to NO donors, S-nitrosoglutathione (GSNO; 150 muM), sodium nitroprussi

125 proaches, we here investigated the effect of S-nitrosoglutathione (GSNO; a physiological NO donor) in

126 The NO donor S:-nitrosoglutathione (GSNO) induced caspase-dependent a

127 nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and arises, at least in sign

128 , allopurinol) or nitric oxide donors (i.e., S-nitrosoglutathione, GSNO).

129 ysteines is insensitive to the inhibition by S-nitrosoglutathione, hydrogen peroxide, or N-ethylmalei

130 we investigated the role of glutathione and S-nitrosoglutathione in animal and human macrophages in

131 , we examined the role of glutathione and/or S-nitrosoglutathione in controlling the growth of intrac

132 inistration of endogenous nitric oxide donor S-nitrosoglutathione in mice blocked the reduction of ex

133 SNO upon exposure to physiological levels of S-nitrosoglutathione in vitro.

134 usside (SNP), 3-morpholinosydnonimine-1, and S-nitrosoglutathione] in P19 stem cells within 4 hr.

135 of HIF-1alpha, whereas NO donors, NOC-18 and S-nitrosoglutathione, increased HIF-1alpha levels.

136 steine and glutathione synthetases to NO and S-nitrosoglutathione indicates that GSH antagonizes the

137 In addition, 8-Br-cGMP and S-nitrosoglutathione induced apoptosis in serum-deprived

138 However, the NO donor S-nitrosoglutathione induced closure of uvr8-1 stomata t

139 oint to different mechanisms by which NO and S-nitrosoglutathione influence cardiac and skeletal musc

140 nitric oxide donors sodium nitroprusside and S-nitrosoglutathione inhibited degranulation, and this e

141 S-Nitrosoglutathione inhibits ornithine decarboxylase by

142 The processing of glutathione and S-nitrosoglutathione is brought about by the action of t

143 trate that the structural isostere of HMGSH, S-nitrosoglutathione, is an ideal hCBR1 substrate (Km =

144 splay excessive accumulation of the NO donor S-nitrosoglutathione, it rescued immunity in nox1 mutant

145 partially S-nitrosated by preincubation with S-nitrosoglutathione, its cardioprotective effect was ma

146 In HEK (human embryonic kidney) cells, S-nitrosoglutathione led to a PKG (protein kinase G)-dep

147 rged supporting that NO and related species (S-nitrosoglutathione, nitro-linolenic acid) are mobile i

148 be due to a direct reaction of proteins with S-nitrosoglutathione or denitrosylation of S-nitrosylate

149 ivation, thus excluding the participation of S-nitrosoglutathione or more oxidizing NO.-derived speci

150 russide and N-acetylcysteine (P = .03) or by S-nitrosoglutathione (P = .004).

151 athione reductase is a negative regulator of S-nitrosoglutathione production) and nitric oxide-induce

152 of human thioredoxin-1 after treatment with S-nitrosoglutathione, providing a high-resolution view o

153 NO/SNO donors such as S-nitrosocysteine and S-nitrosoglutathione readily induced the S-nitrosylation

154 T mice and mice homozygous for a deletion of S-nitrosoglutathione reductase (GSNOR(-/-)), a denitrosy

155 We identified up-regulated S-nitrosoglutathione reductase (GSNOR) as a critical fac

156 S-Nitrosoglutathione reductase (GSNOR) is an alcohol deh

157 S-nitrosoglutathione reductase (GSNOR) represents the be

158 redoxin (Trx) mediated transnitrosylation of S-nitrosoglutathione reductase (GSNOR) underpins the reg

159 Here, we establish that S-nitrosoglutathione reductase (GSNOR), a major protein

160 In this study, we show that S-nitrosoglutathione reductase (GSNOR), a protein key to

161 Here, we show that S-nitrosoglutathione reductase (GSNOR), an enzyme that g

162 erated mice with a targeted gene deletion of S-nitrosoglutathione reductase (GSNOR), and show that th

163 ls deficient in the SNO-metabolizing enzyme, S-nitrosoglutathione reductase (GSNOR), which exhibit en

164 HOT5 encodes S-nitrosoglutathione reductase (GSNOR), which metabolize

165 NO homeostasis is precisely regulated by S-nitrosoglutathione reductase (GSNOR).

166 are controlled in part by the denitrosylase, S-nitrosoglutathione reductase (GSNOR).

167 genetic deletion of the major denitrosylase S-nitrosoglutathione reductase (GSNOR/ADH5).

168 ate assimilation suppresses the redox enzyme S-nitrosoglutathione Reductase 1 (GSNOR1) by S-nitrosyla

169 itrosylation are controlled predominantly by S-nitrosoglutathione reductase 1 (GSNOR1) which turns ov

170 In contrast, knockdown of S-nitrosoglutathione reductase expression had little eff

171 gation, mice with a targeted deletion of the S-nitrosoglutathione reductase gene (GSNOR(-/-)) have re

172 glutathione reductase knockout mouse hearts (S-nitrosoglutathione reductase is a negative regulator o

173 is enabled the profiling of 493 SNO sites in S-nitrosoglutathione reductase knockout hearts.

174 odified cysteine data sets for wild-type and S-nitrosoglutathione reductase knockout mouse hearts (S-

175 accumulation, dendritic cell hyperplasia and S-nitrosoglutathione reductase stimulation being NO-depe

176 of L-arginine dependent NOS-like enzyme and S-nitrosoglutathione reductase were observed under nitra

177 we show that MSCs isolated from mice lacking S-nitrosoglutathione reductase, a denitrosylase that reg

178 d cell expression of thioredoxin-1 (Trx1) or S-nitrosoglutathione reductase, both of which can functi

179 Salmonella virulence in mice, in contrast to S-nitrosoglutathione reductase, flavorubredoxin, or cyto

180 tingn with and mediating redox regulation of S-nitrosoglutathione reductase, which, consistent with p

181 ase-deficient mice-1 [NOS1(-/-)]), and hyper S-nitrosoglutathione reductase-deficient (GSNOR(-/-)) mi

182 Consistent with this cellular phenotype, S-nitrosoglutathione reductase-deficient mice were small

183 WT and S-nitrosoglutathione reductase-deficient MSCs exhibited

184 S-nitrosylation of PPARgamma was elevated in S-nitrosoglutathione reductase-deficient MSCs, diminishi

185 Together, these results reveal that S-nitrosoglutathione reductase-dependent modification of

186 Here, we identify S-nitrosoglutathione-reductase (GSNOR) variants underlyi

187 s-1 (S-nitrosocysteine) and 12,800 M-1 s-1 (S-nitrosoglutathione), respectively, with a stoichiometr

188 ulfides, and could also be glutathiolated by S-nitrosoglutathione resulting in the incorporation of f

189 AF gels indicated that the NO donor compound S-nitrosoglutathione S-nitrosylates significantly more p

190 The results demonstrate that the NO donor S-nitrosoglutathione (S-NO-glutathione) inhibits the sti

191 pounds, S-nitroso-N-acetyl-dl-penicillamine, S-nitrosoglutathione, S-nitrosocaptopril, glucose-S-nitr

192 rolipoic acid, catalyze the denitrosation of S-nitrosoglutathione, S-nitrosocaspase 3, S-nitrosoalbum

193 hieved for low molecular weight RSNOs (i.e., S-nitrosoglutathione, S-nitrosocysteine) by tuning the i

194 acilitate photolysis of nitrosothiols (i.e., S-nitrosoglutathione, S-nitrosocysteine, and S-nitrosoal

195 hydroascorbate, DTNB, lipoic acid/lipoamide, S-nitrosoglutathione, selenodiglutathione, selenite, met

196 bited by the nitric oxide-generating reagent S-nitrosoglutathione (SNG).

197 cytes were treated with either exogenous NO (S-nitrosoglutathione [SNO-GSH]) or a mixture of cytokine

198 The NO donor, S-nitrosoglutathione (SNOG), inhibited, whereas the NOS

199 -S-nitroso-N-acetylpenicillamine (SNAP), and S-nitrosoglutathione (SNOG).

200 ied actin was more readily glutathiolated by S-nitrosoglutathione than by oxidized GSH as determined

201 transpeptidase is to cleave glutathione and S-nitrosoglutathione to the dipeptide (Cys-Gly), which i

202 The addition of the NO donor, S-nitrosoglutathione, to isolated cell lysates or purifi

203 es were specified on 56 distinct proteins in S-nitrosoglutathione-treated (2-10 microM) rat cerebellu

204 the primary source of Sirt1 inhibition upon S-nitrosoglutathione treatment.

205 tif that predicts stable transnitrosation by S-nitrosoglutathione under test conditions, suggesting t

206 S-nitrosoglutathione was highly effective in rapidly red

207 cysteine (SNC) and, to a more modest extent, S-nitrosoglutathione were found to rapidly increase [(3)

208 l-containing tripeptide, exclusively yielded S-nitrosoglutathione when exposed to the NO donor, Et2NN

209 nitric oxide (NO) and superoxide but not by S-nitrosoglutathione which liberates only NO.

210 Interestingly, a small molecule, S-nitrosoglutathione, which is a substrate for gamma glu

211 itrosative defense genes upon treatment with S-nitrosoglutathione, while the mucoid strain PAO578II s