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 by the physiologically relevant nitrosothiol S-nitrosoglutathione.

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

6 activity was potentiated by the presence of 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 t homogenates with the S-nitrosylating agent S-nitrosoglutathione and determined maximal SNO occupanc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 S-Nitrosoglutathione-corrected Delta F508 CFTR exhibited

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 S-Nitrosoglutathione (GSNO) can be electrocatalytically

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 S-Nitrosoglutathione (GSNO) undergoes spontaneous degrad

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

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

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

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

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

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

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

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

89 S-nitrosoglutathione (GSNO), an endogenous bronchodilato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 S-Nitrosoglutathione inhibits ornithine decarboxylase by

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

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

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

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

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

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

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

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

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

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

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

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

145 S-nitrosoglutathione reductase (GSNOR) represents the be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 WT and S-nitrosoglutathione reductase-deficient MSCs exhibited

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 S-nitrosoglutathione was highly effective in rapidly red

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

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

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

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

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