ライフサイエンスコーパス: nitrosothiol

1 of nitric oxide metabolites (ie, nitrite and nitrosothiols).

2 ependent conformational change, to form an S-nitrosothiol.

3 logical response to this biologically active nitrosothiol.

4 teine thiol (or thiolate anion) to form an S-nitrosothiol.

5 th a second NO molecule to produce HNO and a nitrosothiol.

6 form thionitrous acid (HSNO), the smallest S-nitrosothiol.

7 ion that converts a protein Cys thiol to a S-nitrosothiol.

8 m exposure to free *NO but not from cellular nitrosothiol.

9 s encompassing the cellular homeostasis of S-nitrosothiols.

10 s release occurs due to NO liberation from S-nitrosothiols.

11 erate high levels of intracellular protein S-nitrosothiols.

12 al effects of nitric oxide are mediated by S-nitrosothiols.

13 be involved in the regulation of cellular S-nitrosothiols.

14 cellular activity of small molecular weight nitrosothiols.

15 es and the instability of cellular protein S-nitrosothiols.

16 beta subunit (cysbeta-93) to form bioactive nitrosothiols.

17 species and related modifications such as S-nitrosothiols.

18 ult in decreased rates of decomposition of S-nitrosothiols.

19 intracellular glutathione and formation of S-nitrosothiols.

20 and the subsequent formation of NO-donating nitrosothiols.

21 that NO reacts with ---SH groups, forming S-nitrosothiols.

22 anion, the nitric oxide free radical, and S-nitrosothiols.

23 of enzymatic control of cellular thiols and nitrosothiols.

24 lvement of superoxide in the metabolism of S-nitrosothiols.

25 sociated with low concentrations of airway S-nitrosothiols.

26 e reactant that selectively releases NO from nitrosothiols.

27 from reaction of copper(II) thiolates with S-nitrosothiols.

28 ducts, with a decrease in the formation of S-nitrosothiols.

29 e presence of nitrite to form N(2)O(3) and S-nitrosothiols.

30 can be achieved through rational design of S-nitrosothiols.

31 ite versus chemical intermediates, such as S-nitrosothiols.

32 gnificantly higher concentrations of total S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnancy

33 The nitrosothiol 2 was prepared via direct S-nitrosation of

34 ation, did not change total red blood cell S-nitrosothiol abundance but did shift S-nitrosothiol dist

35 manually curated data set of proteins with S-nitrosothiols, accounting for a variety of biochemical f

36 ion of NO provides the fully characterized S-nitrosothiol adduct [Cu(I)](kappa(1)-N(O)SR), which reve

37 s can react with thiols of proteins and form nitrosothiol adducts.

38 S-Nitrosothiol and iron-nitrosyl-protein adducts did not a

39 currently used to quantify putative protein nitrosothiol and N-nitrosamine derivatives.

40 We tested the hypothesis that total S-nitrosothiol and S-nitrosoalbumin concentrations are inc

41 Further reaction of HNO with the remaining S-nitrosothiol and thiol results in the generation of othe

42 ulted in a time-dependent decomposition of S-nitrosothiols and accumulation of nitrite/nitrate in rea

43 Due to combined increases in nitrosothiols and decreases in protein, the preeclampsia

44 Dietary nitrate increased plasma S-nitrosothiols and nitrite, enhanced revascularization, i

45 Nitric oxide, S-nitrosothiols and peroxynitrite are reported to variousl

46 For S-nitrosothiols and peroxynitrite to interfere with the ac

47 f complex I was susceptible to inhibition by nitrosothiols and peroxynitrite.

48 actor for the interaction of the enzyme with nitrosothiols and peroxynitrite.

49 could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological m

50 The role of circulating S-nitrosothiols and SNO-Hb in the regulation of basal vasc

51 hrough exposure to cell membrane-permeable S-nitrosothiols and that sGC is S-nitrosylated and desensi

52 r ascorbate leads to the generation of NO or nitrosothiols and thus stimulates the activation of sGC.

53 s to be more susceptible to NO (especially S-nitrosothiols) and subsequent necrotic cell death.

54 to the anaerobic regulon protected against S-nitrosothiols, and anaerobic growth of E. coli lacking O

55 acellular-reduced glutathione (GSH), protein nitrosothiols, and the activation of the transcription f

56 erin (GTN) and nitric oxide donors such as S-nitrosothiols are clinically vasoactive through stimulat

57 S-Nitrosothiols are known as reagents for NO storage and t

58 Because S-nitrosothiols are known to modify enzymes containing rea

59 studied, the response elements specific to S-nitrosothiols are less clear.

60 S-nitrosothiols are naturally occurring bronchodilators, t

61 Nitrosothiols are ubiquitous molecules that comprise an

62 chanism of inactivation was reported using S-nitrosothiols as the NO donor.

63 to those reported for low-molecular-weight S-nitrosothiols, as well as from nitrite.

64 ndicates that hypoxic vasodilation entails S-nitrosothiol-based (SNO-based) vasoactivity (rather than

65 exploited in the evolutionary development of nitrosothiol-based innate immunity and may provide an av

66 Our results suggest that an S-nitrosothiol-based signal originating from RBCs mediates

67 These observations suggest that S-nitrosothiol biochemistry is of central importance to th

68 cus is on oxidized nitrogen in the form of S-nitrosothiol bond-containing species, which are now appr

69 eased sensitivity to acidified nitrite and S-nitrosothiols, both of which produce nitric oxide.

70 d was evaluated as a fluorescence probe of S-nitrosothiol-bound NO transfer in human umbilical vein e

71 irst gel-based method to identify not only S-nitrosothiols but also other labile NO-based modificatio

72 y of ascorbate to generate a thiol from an S-nitrosothiol, but not from alternatively S-oxidized thio

73 A fraction (25%) was exported as S-nitrosothiol, but this fraction was not increased at low

74 he assay utilizes the catalytic reduction of nitrosothiol by mercuric cation (Hg2+).

75 We have investigated the breakdown of S-nitrosothiols by wild-type (WT) SOD and two common FALS

76 Nitric oxide and S-nitrosothiols can be metabolized by bacteria, but only a

77 howed that exposure to nitric oxide and to S-nitrosothiols causes S-nitrosylation of sGC, which direc

78 m accounts for several unexplained facets of nitrosothiol chemistry in solution, including the observ

79 y binding to cysteine residues and forming S-nitrosothiol complexes.

80 While nitrosothiol compounds have been hypothesized to be impo

81 pment of two methods, for the measurement of nitrosothiol compounds using a chemiluminescence nitric

82 10(-1) microM) and accurate means to measure nitrosothiol concentration in biologic samples.

83 presence of iodine allows estimation of the nitrosothiol concentration.

84 e conclude that S-nitrosoalbumin and total S-nitrosothiol concentrations are significantly increased

85 Tracheal S-nitrosothiol concentrations from eight asthmatic childre

86 re pronounced effect of protecting against S-nitrosothiols, confirms this finding.

87 Erythrocyte S-nitrosothiol content (reflecting mainly S-nitrosohemoglo

88 Compared to similar measurements of total S-nitrosothiol content in bulk solution, use of the microf

89 ys a key role in cellular redox homeostasis, nitrosothiol content in cells, and antiapoptotic signali

90 1+/-25 pmol/mg protein, respectively) when S-nitrosothiol content was expressed per milligram protein

91 lcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygenat

92 ccurs in tandem with increased erythrocyte S-nitrosothiol content, EM, and O2 unloading.

93 IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of the

94 atment with NO donors (increasing cellular S-nitrosothiol contents) substantially enhanced the initia

95 e fluorescence intensity of dansyl-labeled S-nitrosothiols could be enhanced up to 30-fold.

96 tutive NOS activity and generation of NO via nitrosothiol degradation within the first hour.

97 resented >90% of nitrosonium equivalent of S-nitrosothiols degraded during the incubation.

98 RT externalization occurred together in an S-nitrosothiol-dependent and caspase-independent manner.

99 We observed that PDI catalyzes the S-nitrosothiol-dependent oxidation of the heme group of my

100 enitrosylated RBCs than during infusion of S-nitrosothiol-depleted RBCs, and this difference in coron

101 S-nitrosohemoglobin and plasma S-nitrosothiols did not change with NO inhalation.

102 ell S-nitrosothiol abundance but did shift S-nitrosothiol distribution to lower molecular weight spec

103 within endothelial cells from an exogenous S-nitrosothiol donor or from endogenous production of NO b

104 human monocytes as a model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N

105 onse in proportion to the concentration of S-nitrosothiols (e.g., nitrosocysteine, nitrosoglutathione

106 siological levels of nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and ari

107 Nitrosothiol esters of diclofenac comprise a novel class

108 sine monophosphate (cGMP) generation after S-nitrosothiol exposure (65.4 +/- 26.7% reduction compared

109 thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response in

110 The selective S-nitrosothiol formation at Cys-81 led to a doubling of th

111 nvolved both S- and N-nitrosation, and RBC S-nitrosothiol formation emerged as a sensitive indicator

112 r, is much less effective at intracellular S-nitrosothiol formation in the presence of L-cystine or L

113 Nitrosothiol formation in vivo depends not only on the a

114 desensitization and find that heme-assisted nitrosothiol formation of beta1Cys-78 and beta1Cys-122 c

115 GSNO is a low molecular weight SNO (S-nitrosothiol) formed during oxidation of NO.

116 ver, a subsequent incubation of the cells in nitrosothiol-free medium resulted in reconstitution of t

117 atively transferring the thiol groups into S-nitrosothiol functionalities.

118 lytic Cu(II)/(I)-mediated decomposition of S-nitrosothiols generates NO(g) in the thin polymeric film

119 or microsome-associated thiols led to NO or nitrosothiol generation and thus stimulated the activati

120 a NO reaction with cysteine residues to form nitrosothiol groups.

121 ors (including a.NO donor [DeaNonoate], an S-nitrosothiol [GSNO], and the nitroxyl anion donor, Angel

122 Transnitrosation between thiols and S-nitrosothiols has been suggested to be a mechanism of si

123 tanding the biosynthesis and catabolism of S-nitrosothiols has proven to be difficult, in part becaus

124 S-nitrosothiols have been implicated as intermediary trans

125 S-Nitrosothiols have been implicated to play key roles in

126 S-nitrosothiols have been suggested to play an important r

127 Airway S-nitrosothiols have not been studied in asthma.

128 rofluidic sensor to facilitate photolysis of nitrosothiols (i.e., S-nitrosoglutathione, S-nitrosocyst

129 ) assay for measuring picomole quantities of nitrosothiol in biological samples was developed.

130 Both methods were shown to detect nitrosothiols in biological buffers or blood plasma down

131 ve, and specific methods for quantitation of nitrosothiols in biological samples.

132 contention that the transient formation of S-nitrosothiols in biological systems may protect NO from

133 Detection of NO2-, NO3-, and S-nitrosothiols in lung epithelial lining fluids confirmed

134 ) enhanced the therapeutic actions of oral S-nitrosothiols in mouse models of C. difficile infection.

135 trol samples and 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, resp

136 but not SNP or SIN-1, increased levels of S-nitrosothiols in SN56 proteins, consistent with the tran

137 n fraction contained 49.4% of total plasma S-nitrosothiols in the control samples and 53.7% and 56.8%

138 ,we obtained evidence for the formation of S-nitrosothiols in the ER molecule.

139 gnificant increases in nitrite, nitrate, and nitrosothiols in the heart, plasma, and liver.

140 ic analysis showed that the degradation of S-nitrosothiols in the presence of superoxide proceeded at

141 tely accounted for the increased levels of S-nitrosothiols in total plasma.

142 n and storage of NO metabolites (nitrite and nitrosothiols) in the heart.

143 approximately 50% reduction in perfusate [S-nitrosothiol], in association with an increase in perfus

144 of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of e

145 nstituted domain peptides demonstrate that S-nitrosothiols indeed release zinc from both the alpha- a

146 The nitrosothiol intermediate reacts further with RSH to pro

147 lts suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly re

148 tudy, we demonstrate that the transport of S-nitrosothiols is essential for these compounds to affect

149 ay responsible for the cellular effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO),

150 whereas the BJR responses elicited by the S-nitrosothiol, L-S-nitrosocysteine (5 micromol/kg, i.v.),

151 mutated thioredoxin reductase denitrosate S-nitrosothiols less efficiently.

152 thiol uptake, increasing the intracellular S-nitrosothiol level from approximately 60 pmol/mg of prot

153 nitrate, nitrite, and low-molecular-weight S-nitrosothiol levels by chemiluminescence.

154 uction of NO was paralleled by a decrease in nitrosothiol levels for 2 hour, suggesting that immediat

155 lysis, this device was used to measure basal nitrosothiol levels from the vasculature of a healthy po

156 ovide new insight into the determinants of S-nitrosothiol levels in subcellular compartments.

157 ne biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a cons

158 estored intracardiac nitrite and increased S-nitrosothiol levels, decreased pathological cardiac mito

159 was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residues,

160 c oxide synthase expression, and nitrite and nitrosothiol levels.

161 t resulting in 100-fold higher intracellular nitrosothiol levels.

162 In parallel, S-nitrosothiol-linked probes enable enrichment and detecti

163 the detection of other low-molecular weight nitrosothiols (LMW-RSNOs) in biological samples.

164 cordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, pertu

165 We suggest that S-nitrosothiol metabolism may be a target for the developm

166 nts a potential physiological mechanism of S-nitrosothiol metabolism.

167 and provide insight into the aetiology of S-nitrosothiols, methaemoglobin and its related valency hy

168 Importantly, S-nitrosothiol-MIF formation was measured both in vitro an

169 This decrease was paralleled by a S-nitrosothiol-MIF- but not Cys81 serine (Ser)-MIF mutant-

170 the catalytic site and that nitric oxide (or nitrosothiols) might act as a negative regulator of V-AT

171 versies surrounding the proposal that this S-nitrosothiol modulates blood flow in vivo.

172 cubated with cysteine, suggesting that these nitrosothiols must react with cysteine to form CSNO, whi

173 bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated he

174 In addition to nitrosothiol, nitrite and atmospheric nitrogen oxides ar

175 one marrow-derived CD31(+)/CD45(-), plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP levels

176 isulfide acts as a source of nitrosonium for nitrosothiol nitrosation, completing the catalytic cycle

177 ulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a versat

178 mass spectrometry, we found that NO forms S-nitrosothiols on Cys67 and Cys95 of HIV-PR which directl

179 d method for analyzing protein and peptide S-nitrosothiols on gels using the fluorescent probes 4,5-d

180 se of NO occurs either from both nitrite and nitrosothiols or from nitrite alone, respectively.

181 gical event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies com

182 However, the mechanisms by which an S-nitrosothiol (or the S-nitroso functional group) is tran

183 e data demonstrate for the first time that S-nitrosothiols oxidatively modify PTEN, leading to revers

184 ption and corresponding delivery of plasma S-nitrosothiols (P>0.05).

185 y, with a stoichiometric ratio of 1 mol of S-nitrosothiol per 2 mol of superoxide.

186 y effected by NO(g) with the use of trityl-S-nitrosothiol (Ph3CSNO) as the nitric oxide source.

187 ripheral circulation, and (iii) SNO-Hb and S-nitrosothiols play a minimal role in the regulation of b

188 l concentrations of nitrite and deoxyHb, a S-nitrosothiol precursor is formed within seconds and prod

189 onic chain mechanism in which nitrosation of nitrosothiol produces a nitrosated cation that, in turn,

190 Here we demonstrate that sulfinic acids and nitrosothiols react to form a stable thiosulfonate bond,

191 emical mechanism by which nitric oxide and S-nitrosothiols react with cysteine residues in ornithine

192 vivo Using this approach, called SNOxICAT (S-nitrosothiol redox isotope-coded affinity tag), we found

193 y slower reaction rates of superoxide with S-nitrosothiols relative to the reaction rate with NO are

194 can be preserved in a more stable form of S-nitrosothiols (RS-NO).

195 N) that leads to S-nitrosation to give the S-nitrosothiol RSNO and copper(II) hydroxide [Cu(II)]-OH.

196 study, we examined the chemical pathways of nitrosothiol (RSNO) production at low micromolar concent

197 The decomposition of S-nitrosothiols (RSNO) in solution under oxidative conditi

198 oxidation leads to formation of vasoactive S-nitrosothiols (RSNO) in vitro and in vivo as detected el

199 Nitrosothiols (RSNO), formed from thiols and metabolites

200 metabolites with thiols and metals to form S-nitrosothiols (RSNOs) and metal nitrosyls.

201 S-Nitrosothiols (RSNOs) are carriers of nitric oxide (NO)

202 S-Nitrosothiols (RSNOs) are important exogenous and endoge

203 Amperometric detection of S-nitrosothiols (RSNOs) at submicromolar levels in blood s

204 Although S-nitrosothiols (RSNOs) have been frequently implicated in

205 Nitrosothiols (RSNOs) have been proposed as important in

206 dely used methodology for the detection of S-nitrosothiols (RSNOs) in biological samples.

207 S-nitrosothiols (RSNOs) serve as ready sources of biologic

208 The concentration of S-nitrosothiols (RSNOs), endogenous transporters of the si

209 with the low molecular mass cell-permeable S-nitrosothiol S-nitrosocysteine ethyl ester (SNCEE).

210 nd inhibited by the physiologically relevant nitrosothiol S-nitrosoglutathione.

211 ein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1B

212 the specific transport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomocys

213 ries of novel diclofenac esters containing a nitrosothiol (-S-NO) moiety as a NO donor functionality

214 dues in ornithine decarboxylase to form an S-nitrosothiol(s) on the protein.

215 GGT also metabolizes the naturally occurring nitrosothiol, S-nitrosoglutathione (GSNO).

216 fore, a reference sample, which includes the nitrosothiol sample and all reagents except Hg2+, is uti

217 eric nitrogen oxides which "contaminate" the nitrosothiol sample and reagents.

218 te activation and is the precursor of NO and nitrosothiols, serving as the link between organic nitra

219 ransformation and is the precursor of NO and nitrosothiols, serving as the link between organic nitra

220 te that zinc thiolate bonds are targets of S-nitrosothiol signaling and further indicate that MT-III

221 b) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused r

222 ses the rate at which low-molecular-weight S-nitrosothiol (SNO) decomposes in vitro.

223 The role of S-nitrosothiol (SNO) formation and turnover in governing N

224 S-nitrosothiol (SNO) formation was increased in isoprotere

225 Disruption of S-nitrosothiol (SNO) homeostasis may result not only from

226 Here we utilize antibodies specific for the nitrosothiol (SNO) moiety to provide an immunohistochemi

227 Further, this Trx S-nitrosothiol (SNO) reductase activity was potentiated fo

228 in human erythrocytes haemoglobin-derived S-nitrosothiol (SNO), generated from imported NO, is assoc

229 etaCys93) that has been assigned a role in S-nitrosothiol (SNO)-based hypoxic vasodilation by RBCs.

230 S-nitrosothiol (SNO)-deficient RBCs produce impaired vasod

231 ety to a protein cysteine thiol forming an S-nitrosothiol (SNO).

232 ety to a protein cysteine thiol to form an S-nitrosothiol (SNO).

233 steine thiol by an NO group to generate an S-nitrosothiol (SNO).

234 10(-4) at 3 h vs. 6.5 x 10(-4) (fresh) mol S-nitrosothiol (SNO)/mol Hb tetramer (P = 0.032, mercuric-

235 ed 1,276 S-nitrosylated cysteine residues [S-nitrosothiol (SNO)] on 491 proteins in resting hearts fr

236 We demonstrate here that S-nitrosothiols (SNO) caused a dose-dependent inhibition o

237 mical reaction products [nitrite, nitrate, S-nitrosothiols (SNO), and nitrotyrosine] before, immediat

238 digm is well exemplified in bacteria where S-nitrosothiols (SNO)-compounds identified with antimicrob

239 achment of NO to cysteine residues to form S-nitrosothiols (SNO).

240 n (iron nitrosyl, FeNO) to cysteine thiol (S-nitrosothiol, SNO) that subserves bioactivation, and in

241 a family of NO-related molecules and that S-nitrosothiols (SNOs) are central to signal transduction

242 Nitric oxide (NO) and/or S-nitrosothiols (SNOs) can prevent the loss of beta-AR sig

243 ereas treatments favoring stabilization of S-nitrosothiols (SNOs) decreased its cytotoxic potency.

244 e that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a varie

245 emical data demonstrate a pivotal role for S-nitrosothiols (SNOs) in mediating the actions of nitric

246 ly through protein S-nitrosylation to form S-nitrosothiols (SNOs) in target proteins, operates coordi

247 ehydrogenase involved in the regulation of S-nitrosothiols (SNOs) in vivo.

248 rd nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in pathog

249 S-nitrosothiols (SNOs), formed by nitric oxide (NO)-mediat

250 dified the biotin switch assay for protein S-nitrosothiols (SNOs), using resin-assisted capture (SNO-

251 NO bioactivity is packaged in the form of S-nitrosothiols (SNOs), which are relatively resistant to

252 synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identifie

253 reductase (GSNOR) and are depleted of lung S-nitrosothiols (SNOs).

254 r of NO from Hb to form other (vasoactive) S-nitrosothiols (SNOs).

255 ) is signalled by deoxyhaemoglobin-derived S-nitrosothiols (SNOs).

256 activity in mammals is largely mediated by S-nitrosothiols (SNOs).

257 sylation by biologically relevant low-mass S-nitrosothiols (SNOs).

258 The direct amperometric detection of S-nitrosothiol species (RSNOs) is realized by modifying a

259 source of this NO is the already available S-nitrosothiol store rather than de novo synthesis by NOS.

260 through intracellular NO by modulation of S-nitrosothiol stores and stimulation of NOS activity.

261 nction as a generator for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as such,

262 Other nitrosothiols such as S-nitrosoglutathione are not subst

263 to cause vasodilation as compared to other S-nitrosothiols suggests potential application in biologic

264 data provide evidence for a physiological S-nitrosothiol synthase activity of tetrameric Hb that dep

265 NO can be converted into nitrite or nitrosothiols that are stable until cleaved by UV to rel

266 We hypothesized that nitrosothiols that promote protein S-nitrosylation would

267 thiols was used to explore the kinetics of S-nitrosothiol/thiol transnitrosation and was evaluated as

268 NO2) intermediate and yields low levels of S-nitrosothiols (thionitrites; RSNO), both of which are th

269 that a single sulfinic acid can react with a nitrosothiol to form a thiosulfonate linkage.

270 d cation that, in turn, reacts with a second nitrosothiol to produce nitrosated disulfide and the NO

271 in the enzyme active site on the sulfur of S-nitrosothiols to form a mixed disulfide between the inac

272 Here, we report that H(2)S reacts with S-nitrosothiols to form thionitrous acid (HSNO), the small

273 luded ultraviolet-induced decomposition of S-nitrosothiols to liberate NO captured by a florigenic re

274 This reaction converts unstable primary S-nitrosothiols to stable disulfide-iminophosphorane produ

275 mational changes in the toxin enabled host S-nitrosothiols to transnitrosylate the toxin catalytic cy

276 However, the mechanisms by which S-nitrosothiols transduce their activity across cell membr

277 to be incompatible with life were all the S-nitrosothiols transformed into bioactive equivalents dur

278 this study, we have examined the effect of S-nitrosothiol transport on intracellular thiol status and

279 -20x improvement in sensitivity depending on nitrosothiol type).

280 sence of L-cystine enhanced GSNO-dependent S-nitrosothiol uptake, increasing the intracellular S-nitr

281 A bis-ligation reaction of S-nitrosothiols using triaryl substituted phosphine-thioes

282 The resultant protein-S-nitrosothiol was found to be unstable and to decompose s

283 The inhibition of papain by S-nitrosothiol was rapidly reversed by dithiothreitol, but

284 Intracellular accumulation of S-nitrosothiols was observed with 2a but not with 2b.

285 ed by yeast flavohemoglobin against NO and S-nitrosothiols was seen under both anaerobic and aerobic

286 In addition, one of the dansyl-labeled S-nitrosothiols was used to explore the kinetics of S-nitr

287 To selectively measure nitrosothiols, we developed a redox quinone-hydroquinone

288 kground nitrite and stabilizes erythrocyte S-nitrosothiols, we find the levels of SNO-Hb in the basal

289 nitrate, nitrite, and low-molecular-weight S-nitrosothiol were in the normal range; however, enhanced

290 S-Nitrosothiols were barely detectable.

291 Moreover, a variety of additional S-nitrosothiols were catabolized more readily by A4V SOD t

292 Surprisingly, when concentrations of S-nitrosothiols were high, nitric oxide function also gove

293 A series of fluorophore-labeled S-nitrosothiols were synthesized, and their fluorescence e

294 We found that low-molecular-weight S-nitrosothiols were undetectable and S-nitroso-albumin le

295 ficantly more reactive than MT-I/II toward S-nitrosothiols, whereas the reactivity of all three isofo

296 is reflected in the level of intracellular S-nitrosothiols, which are constitutively metabolized.

297 wed by reductive generation of thiols from S-nitrosothiols, which are then labeled with either a biot

298 nism, we here investigate the reactions of S-nitrosothiols with different isoforms of MT.

299 and thiols, furnishing iron nitrosyls and S-nitrosothiols with wide-ranging stabilities and reactivi

300 nges that occur after exposure of cells to S-nitrosothiol, with respect to thiol chemistry, are disti

301 g reactive cysteines, we hypothesized that S-nitrosothiols would oxidize PTEN and inhibit its phospha