ライフサイエンスコーパス: S-nitrosothiol

1 -dependent conformational change, to form an S-nitrosothiol.

2 ysteine thiol (or thiolate anion) to form an S-nitrosothiol.

3 iate reduces an electron acceptor to produce S-nitrosothiol.

4 ion-catalyzed decomposition than the parent S-nitrosothiol.

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

6 ction that converts a protein Cys thiol to a S-nitrosothiol.

7 ical effects of nitric oxide are mediated by S-nitrosothiols.

8 ay be involved in the regulation of cellular S-nitrosothiols.

9 obes and the instability of cellular protein S-nitrosothiols.

10 ur species and related modifications such as S-nitrosothiols.

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

12 esult in decreased rates of decomposition of S-nitrosothiols.

13 f intracellular glutathione and formation of S-nitrosothiols.

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

15 volvement of superoxide in the metabolism of S-nitrosothiols.

16 associated with low concentrations of airway S-nitrosothiols.

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

18 ted in release of nitric oxide (NO) from the S-nitrosothiols.

19 in is promoted by the erythrocytic export of S-nitrosothiols.

20 ric methods for the reliable quantitation of S-nitrosothiols.

21 roducts, with a decrease in the formation of S-nitrosothiols.

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

23 y can be achieved through rational design of S-nitrosothiols.

24 trite versus chemical intermediates, such as S-nitrosothiols.

25 sms encompassing the cellular homeostasis of S-nitrosothiols.

26 his release occurs due to NO liberation from S-nitrosothiols.

27 enerate high levels of intracellular protein S-nitrosothiols.

28 significantly higher concentrations of total S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnan

29 osation, did not change total red blood cell S-nitrosothiol abundance but did shift S-nitrosothiol di

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

31 ition of NO provides the fully characterized S-nitrosothiol adduct [Cu(I)](kappa(1)-N(O)SR), which re

32 S-Nitrosothiol and iron-nitrosyl-protein adducts did not

33 We tested the hypothesis that total S-nitrosothiol and S-nitrosoalbumin concentrations are i

34 Further reaction of HNO with the remaining S-nitrosothiol and thiol results in the generation of ot

35 iol groups of proteins to give corresponding S-nitrosothiols and 5-thio-2-nitrobenzoate dianion.

36 esulted in a time-dependent decomposition of S-nitrosothiols and accumulation of nitrite/nitrate in r

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

38 Nitric oxide, S-nitrosothiols and peroxynitrite are reported to variou

39 For S-nitrosothiols and peroxynitrite to interfere with the

40 n could facilitate nitric oxide release from S-nitrosothiols and represents a potential physiological

41 The role of circulating S-nitrosothiols and SNO-Hb in the regulation of basal va

42 through exposure to cell membrane-permeable S-nitrosothiols and that sGC is S-nitrosylated and desen

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

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

45 ycerin (GTN) and nitric oxide donors such as S-nitrosothiols are clinically vasoactive through stimul

46 S-Nitrosothiols are known as reagents for NO storage and

47 Because S-nitrosothiols are known to modify enzymes containing r

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

49 S-nitrosothiols are naturally occurring bronchodilators,

50 S-Nitrosothiols are stable compounds at 37 degrees C and

51 mechanism of inactivation was reported using S-nitrosothiols as the NO donor.

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

53 indicates that hypoxic vasodilation entails S-nitrosothiol-based (SNO-based) vasoactivity (rather th

54 Our results suggest that an S-nitrosothiol-based signal originating from RBCs mediat

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

56 focus is on oxidized nitrogen in the form of S-nitrosothiol bond-containing species, which are now ap

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

58 and was evaluated as a fluorescence probe of S-nitrosothiol-bound NO transfer in human umbilical vein

59 first gel-based method to identify not only S-nitrosothiols but also other labile NO-based modificat

60 ity of ascorbate to generate a thiol from an S-nitrosothiol, but not from alternatively S-oxidized th

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

62 and ascorbate can stimulate decomposition of S-nitrosothiol by chemical reduction of contaminating tr

63 nonaphthalene and nitrous acid released from S-nitrosothiols by treatment with mercuric chloride in a

64 100% as documented by simultaneous assays of S-nitrosothiols by uv spectrophotometry and by Saville m

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

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

67 We find that S-nitrosothiols can react with thiols to generate nitrox

68 showed that exposure to nitric oxide and to S-nitrosothiols causes S-nitrosylation of sGC, which dir

69 by binding to cysteine residues and forming S-nitrosothiol complexes.

70 We conclude that S-nitrosoalbumin and total S-nitrosothiol concentrations are significantly increase

71 Tracheal S-nitrosothiol concentrations from eight asthmatic child

72 Mean S-nitrosothiol concentrations in asthmatic children were

73 more pronounced effect of protecting against S-nitrosothiols, confirms this finding.

74 Erythrocyte S-nitrosothiol content (reflecting mainly S-nitrosohemog

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

76 151+/-25 pmol/mg protein, respectively) when S-nitrosothiol content was expressed per milligram prote

77 tylcysteine (SNOAC), decreasing erythrocytic S-nitrosothiol content, both during whole-blood deoxygen

78 occurs in tandem with increased erythrocyte S-nitrosothiol content, EM, and O2 unloading.

79 IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of th

80 reatment with NO donors (increasing cellular S-nitrosothiol contents) substantially enhanced the init

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

82 The mechanism and products of S-nitrosothiol decomposition are of great significance t

83 Transnitrosation can also stimulate S-nitrosothiol decomposition if the product S-nitrosothi

84 The biological relevance of S-nitrosothiol decomposition is discussed.

85 epresented >90% of nitrosonium equivalent of S-nitrosothiols degraded during the incubation.

86 CRT externalization occurred together in an S-nitrosothiol-dependent and caspase-independent manner.

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

88 renitrosylated RBCs than during infusion of S-nitrosothiol-depleted RBCs, and this difference in cor

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

90 cell S-nitrosothiol abundance but did shift S-nitrosothiol distribution to lower molecular weight sp

91 m within endothelial cells from an exogenous S-nitrosothiol donor or from endogenous production of NO

92 sponse in proportion to the concentration of S-nitrosothiols (e.g., nitrosocysteine, nitrosoglutathio

93 hysiological levels of nitric oxide (NO) and S-nitrosothiols (e.g., S-nitrosoglutathione, GSNO) and a

94 nosine monophosphate (cGMP) generation after S-nitrosothiol exposure (65.4 +/- 26.7% reduction compar

95 e thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response

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

97 involved both S- and N-nitrosation, and RBC S-nitrosothiol formation emerged as a sensitive indicato

98 nor, is much less effective at intracellular S-nitrosothiol formation in the presence of L-cystine or

99 is study was to investigate the mechanism of S-nitrosothiol formation under physiological conditions.

100 presented for the quantitative detection of S-nitrosothiols formed by model biological thiols, cyste

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

102 itatively transferring the thiol groups into S-nitrosothiol functionalities.

103 talytic Cu(II)/(I)-mediated decomposition of S-nitrosothiols generates NO(g) in the thin polymeric fi

104 ators (including a.NO donor [DeaNonoate], an S-nitrosothiol [GSNO], and the nitroxyl anion donor, Ang

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

106 rstanding the biosynthesis and catabolism of S-nitrosothiols has proven to be difficult, in part beca

107 S-nitrosothiols have been implicated as intermediary tra

108 S-Nitrosothiols have been implicated to play key roles i

109 S-nitrosothiols have been shown to affect a number of ph

110 S-nitrosothiols have been suggested to play an important

111 S-Nitrosothiols have generated considerable interest due

112 S-Nitrosothiols have many biological activities and have

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

114 ions .NO reacts directly with thiols to form S-nitrosothiol in the presence of an electron acceptor.

115 e contention that the transient formation of S-nitrosothiols in biological systems may protect NO fro

116 que offers simple and rapid determination of S-nitrosothiols in complex reaction mixtures with the de

117 Detection of NO2-, NO3-, and S-nitrosothiols in lung epithelial lining fluids confirm

118 (6) enhanced the therapeutic actions of oral S-nitrosothiols in mouse models of C. difficile infectio

119 ontrol samples and 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, re

120 In analysis of S-nitrosothiols in protein-containing mixtures, HgCl2-me

121 P, but not SNP or SIN-1, increased levels of S-nitrosothiols in SN56 proteins, consistent with the tr

122 min fraction contained 49.4% of total plasma S-nitrosothiols in the control samples and 53.7% and 56.

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

124 etic analysis showed that the degradation of S-nitrosothiols in the presence of superoxide proceeded

125 letely accounted for the increased levels of S-nitrosothiols in total plasma.

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

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

128 constituted domain peptides demonstrate that S-nitrosothiols indeed release zinc from both the alpha-

129 mine whether the hemodynamic effects of this S-nitrosothiol involves the activation of stereoselectiv

130 Finally, the formation of S-nitrosothiol is demonstrated in an anaerobic environme

131 S-nitrosothiol decomposition if the product S-nitrosothiol is more susceptible to transition metal i

132 Concentration of S-nitrosothiols is determined from the difference in flu

133 sults suggest that inactivation of papain by S-nitrosothiols is due to a direct attack of the highly

134 study, we demonstrate that the transport of S-nitrosothiols is essential for these compounds to affe

135 ed in the modification of the thiol group by S-nitrosothiols is important for understanding the role

136 hway responsible for the cellular effects of S-nitrosothiols is specific for S-nitrosocysteine (CSNO)

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

138 th mutated thioredoxin reductase denitrosate S-nitrosothiols less efficiently.

139 sothiol uptake, increasing the intracellular S-nitrosothiol level from approximately 60 pmol/mg of pr

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

141 provide new insight into the determinants of S-nitrosothiol levels in subcellular compartments.

142 eine biosynthesis pathway and an increase in S-nitrosothiol levels suggest S-nitrosylation to be a co

143 restored intracardiac nitrite and increased S-nitrosothiol levels, decreased pathological cardiac mi

144 s was accompanied by an increase in cellular S-nitrosothiol levels, modification of cysteines residue

145 In parallel, S-nitrosothiol-linked probes enable enrichment and detec

146 ocysteine-sensitive metH gene indicated that S-nitrosothiols may directly deplete intracellular homoc

147 Accordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, per

148 We suggest that S-nitrosothiol metabolism may be a target for the develo

149 sents a potential physiological mechanism of S-nitrosothiol metabolism.

150 e, and provide insight into the aetiology of S-nitrosothiols, methaemoglobin and its related valency

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

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

153 roversies surrounding the proposal that this S-nitrosothiol modulates blood flow in vivo.

154 Reduced metal ion (e.g. Cu+) decomposes S-nitrosothiols more rapidly than oxidized metal ion (e.

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

156 bone marrow-derived CD31(+)/CD45(-), plasma S-nitrosothiols, nitrite, and skeletal tissue cGMP level

157 egulated by redox reactions involving NO and S-nitrosothiols (nitrosative stress), emphasizing a vers

158 de that in the HEK293 expression system, the S-nitrosothiol NO donors inhibit L-type Ca2+ channels by

159 um conferred specific hypersusceptibility to S-nitrosothiol NO-donor compounds and attenuated virulen

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

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

162 logical event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies c

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

164 ese data demonstrate for the first time that S-nitrosothiols oxidatively modify PTEN, leading to reve

165 umption and corresponding delivery of plasma S-nitrosothiols (P>0.05).

166 ely, with a stoichiometric ratio of 1 mol of S-nitrosothiol per 2 mol of superoxide.

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

168 peripheral circulation, and (iii) SNO-Hb and S-nitrosothiols play a minimal role in the regulation of

169 cal concentrations of nitrite and deoxyHb, a S-nitrosothiol precursor is formed within seconds and pr

170 The potential physiological importance of S-nitrosothiols prompted us to examine their reaction wi

171 chemical mechanism by which nitric oxide and S-nitrosothiols react with cysteine residues in ornithin

172 ovide tentative evidence that membrane-bound S-nitrosothiol receptors may exist within the cardiovasc

173 l involves the activation of stereoselective S-nitrosothiol receptors within the cardiovascular syste

174 involve its interaction with stereoselective S-nitrosothiol recognition sites within the vasculature

175 n vivo Using this approach, called SNOxICAT (S-nitrosothiol redox isotope-coded affinity tag), we fou

176 lly slower reaction rates of superoxide with S-nitrosothiols relative to the reaction rate with NO ar

177 S-Nitrosothiol resistance was restored by exogenous homo

178 Photolysis of S-nitrosothiols results in the formation of .NO and disu

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

180 O2N) that leads to S-nitrosation to give the S-nitrosothiol RSNO and copper(II) hydroxide [Cu(II)]-OH

181 The decomposition of S-nitrosothiols (RSNO) in solution under oxidative condi

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

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

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

185 S-Nitrosothiols (RSNOs) are important exogenous and endo

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

187 Although S-nitrosothiols (RSNOs) have been frequently implicated

188 Here we report that certain S-nitrosothiols (RSNOs) impose what we term a "nitrosati

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

190 S-nitrosothiols (RSNOs) serve as ready sources of biolog

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

192 ested the effects of one class of NO donors, S-nitrosothiols (RSNOs), on expressed cardiovascular L-t

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

194 otein S-nitrosylation, the colocalization of S-nitrosothiol (S-NO) and protein-tyrosine phosphatase 1

195 t the specific transport of amino acid-based S-nitrosothiols (S-nitroso-L-cysteine and S-nitrosohomoc

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

197 rate that zinc thiolate bonds are targets of S-nitrosothiol signaling and further indicate that MT-II

198 tHb) on HPV, expired NO (eNO), and perfusate S-nitrosothiol (SNO) concentration in isolated, perfused

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

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

201 S-nitrosothiol (SNO) formation was increased in isoprote

202 Disruption of S-nitrosothiol (SNO) homeostasis may result not only fro

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

204 at in human erythrocytes haemoglobin-derived S-nitrosothiol (SNO), generated from imported NO, is ass

205 (betaCys93) that has been assigned a role in S-nitrosothiol (SNO)-based hypoxic vasodilation by RBCs.

206 S-nitrosothiol (SNO)-deficient RBCs produce impaired vas

207 oiety to a protein cysteine thiol to form an S-nitrosothiol (SNO).

208 cysteine thiol by an NO group to generate an S-nitrosothiol (SNO).

209 oiety to a protein cysteine thiol forming an S-nitrosothiol (SNO).

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

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

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

213 hemical reaction products [nitrite, nitrate, S-nitrosothiols (SNO), and nitrotyrosine] before, immedi

214 radigm is well exemplified in bacteria where S-nitrosothiols (SNO)-compounds identified with antimicr

215 ttachment of NO to cysteine residues to form S-nitrosothiols (SNO).

216 ron (iron nitrosyl, FeNO) to cysteine thiol (S-nitrosothiol, SNO) that subserves bioactivation, and i

217 es a family of NO-related molecules and that S-nitrosothiols (SNOs) are central to signal transductio

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

219 whereas treatments favoring stabilization of S-nitrosothiols (SNOs) decreased its cytotoxic potency.

220 nce that nitric oxide (NO) and/or endogenous S-nitrosothiols (SNOs) exert protective effects in a var

221 chemical data demonstrate a pivotal role for S-nitrosothiols (SNOs) in mediating the actions of nitri

222 ntly through protein S-nitrosylation to form S-nitrosothiols (SNOs) in target proteins, operates coor

223 dehydrogenase involved in the regulation of S-nitrosothiols (SNOs) in vivo.

224 ward nitric oxide (NO) leads to formation of S-nitrosothiols (SNOs) that play important roles in path

225 S-nitrosothiols (SNOs), formed by nitric oxide (NO)-medi

226 modified the biotin switch assay for protein S-nitrosothiols (SNOs), using resin-assisted capture (SN

227 st NO bioactivity is packaged in the form of S-nitrosothiols (SNOs), which are relatively resistant t

228 de synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identif

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

230 fer of NO from Hb to form other (vasoactive) S-nitrosothiols (SNOs).

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

232 ioactivity in mammals is largely mediated by S-nitrosothiols (SNOs).

233 rosylation by biologically relevant low-mass S-nitrosothiols (SNOs).

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

235 e source of this NO is the already available S-nitrosothiol store rather than de novo synthesis by NO

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

237 function as a generator for the formation of S-nitrosothiols such as S-nitrosoglutathione and, as suc

238 y to cause vasodilation as compared to other S-nitrosothiols suggests potential application in biolog

239 ur data provide evidence for a physiological S-nitrosothiol synthase activity of tetrameric Hb that d

240 sothiols was used to explore the kinetics of S-nitrosothiol/thiol transnitrosation and was evaluated

241 RSNO2) intermediate and yields low levels of S-nitrosothiols (thionitrites; RSNO), both of which are

242 ffers) stimulates the catalytic breakdown of S-nitrosothiols to .NO and disulfide.

243 -nitroso-L-cysteine (1) and six other simple S-nitrosothiols to Cys 34 of bovine serum albumin (2) ha

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

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

246 ncluded ultraviolet-induced decomposition of S-nitrosothiols to liberate NO captured by a florigenic

247 This reaction converts unstable primary S-nitrosothiols to stable disulfide-iminophosphorane pro

248 ormational changes in the toxin enabled host S-nitrosothiols to transnitrosylate the toxin catalytic

249 However, the mechanisms by which S-nitrosothiols transduce their activity across cell mem

250 as to be incompatible with life were all the S-nitrosothiols transformed into bioactive equivalents d

251 n this study, we have examined the effect of S-nitrosothiol transport on intracellular thiol status a

252 resence of L-cystine enhanced GSNO-dependent S-nitrosothiol uptake, increasing the intracellular S-ni

253 A bis-ligation reaction of S-nitrosothiols using triaryl substituted phosphine-thio

254 urate determination of low concentrations of S-nitrosothiols, utilizing conventional spectroscopic te

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

256 The inhibition of papain by S-nitrosothiol was rapidly reversed by dithiothreitol, b

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

258 rred by yeast flavohemoglobin against NO and S-nitrosothiols was seen under both anaerobic and aerobi

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

260 ackground nitrite and stabilizes erythrocyte S-nitrosothiols, we find the levels of SNO-Hb in the bas

261 a nitrate, nitrite, and low-molecular-weight S-nitrosothiol were in the normal range; however, enhanc

262 S-Nitrosothiols were barely detectable.

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

264 Surprisingly, when concentrations of S-nitrosothiols were high, nitric oxide function also go

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

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

267 nificantly more reactive than MT-I/II toward S-nitrosothiols, whereas the reactivity of all three iso

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

269 lowed by reductive generation of thiols from S-nitrosothiols, which are then labeled with either a bi

270 hanism, we here investigate the reactions of S-nitrosothiols with different isoforms of MT.

271 on and thiols, furnishing iron nitrosyls and S-nitrosothiols with wide-ranging stabilities and reacti

272 hanges that occur after exposure of cells to S-nitrosothiol, with respect to thiol chemistry, are dis

273 ing reactive cysteines, we hypothesized that S-nitrosothiols would oxidize PTEN and inhibit its phosp