ライフサイエンスコーパス: glutathionylation

1 e to cysteine residues in target proteins (S-glutathionylation).

2 esults confirm that Grx2 deactivates UCP3 by glutathionylation.

3 ted neutrophils via driving reversible actin glutathionylation.

4 release (CICR) via the IP(3)R is enhanced by glutathionylation.

5 nts pyridine disulfides (PDSs), suggesting S-glutathionylation.

6 in-glutathione (P-SSG) mixed disulfide, i.e. glutathionylation.

7 annel is inhibited in oxidative stress via S-glutathionylation.

8 e stress could alter eNOS activity through S-glutathionylation.

9 utathione S-transferase A4 (GSTA4) dependent glutathionylation.

10 C91A mutation, presumably by preventing C91 glutathionylation.

11 ecific reducing agents, which reverse this S-glutathionylation.

12 mass increase [+305.3 Da] consistent with S-glutathionylation.

13 steine-dependent activities are modulated by glutathionylation.

14 as operating as a thiol donor with minimal S-glutathionylation.

15 proximal DNA-binding domain, as the sites of glutathionylation.

16 attached to the E2 subunit, was the site of glutathionylation.

17 quences of alpha-ketoglutarate dehydrogenase glutathionylation.

18 cysteine residue, Cys(90), was involved in S-glutathionylation.

19 get for oxidative inactivation by means of S-glutathionylation.

20 so major sites of both S-nitrosylation and S-glutathionylation.

21 s, revealed that the channel is activated by glutathionylation.

22 ion, limited nitration, and high levels of S-glutathionylation.

23 nase was rapidly and reversibly inhibited by glutathionylation.

24 tion by an oxidative mechanism, specifically glutathionylation.

25 oxin 1 in patch pipette solutions to reverse glutathionylation.

26 the yeast glutathione S-transferase Gtt1p in glutathionylation.

27 eins, most of which are novel candidates for glutathionylation.

28 yn, were then confirmed to be susceptible to glutathionylation.

29 xidative modification of cysteine known as S-glutathionylation.

30 viding a versatile handle for characterizing glutathionylation.

31 reactive thiol in human MCU that undergoes S-glutathionylation.

32 ntracellular GSH:GSSG ratio and cause eNOS S-glutathionylation.

33 otting and the direct determination of total glutathionylation.

34 athione, or certain metals, NO can lead to S-glutathionylation, a post-translational modification pot

35 iated proton leak is modulated by reversible glutathionylation, a process responsive to small changes

36 sulfenic acid-dependent switch, leading to S-glutathionylation, a protein modification that protects

37 Protein thiols can undergo S-glutathionylation, a reversible protein modification inv

38 ced hypertension was associated with Sirt3 S-glutathionylation, acetylation of vascular SOD2, and red

39 s of the 19 S regulatory particle, undergo S-glutathionylation after exposure of purified 26 S protea

40 ion, intramolecular disulfide formation, and glutathionylation, allowing accumulation of its substrat

41 r than oxidation to sulfonic acid, such as S-glutathionylation, also decreased aconitase activity, th

42 ound to trigger both GAPDH nitrosylation and glutathionylation, although nitrosylation was widely pro

43 hat eNOS uncoupling can also be induced by S-glutathionylation, although the functional relationships

44 Titin has been identified as a target of S-glutathionylation, an end product of the nitric-oxide-si

45 hese cysteines to alanine leads to a loss in glutathionylation and a concomitant loss in calcium chan

46 The C91A mutation limits MAL glutathionylation and acts as a dominant negative, block

47 ed technique to identify proteins undergoing glutathionylation and apply it to the secretome and the

48 We found that oxidant-induced increased S-glutathionylation and calcium-independent puncta formati

49 ty appears to be modulated through enzymatic glutathionylation and deglutathionylation.

50 ngly suggest that oxidative damage-induced S-glutathionylation and degradation of TK2 have significan

51 We further investigated the mechanism of glutathionylation and demonstrate a role for the yeast g

52 ed LysM(iDTR) transgenic mice prevented eNOS glutathionylation and eNOS-derived N(omega)-nitro-L-argi

53 Thus, the decreasing S-glutathionylation and ETA in mitochondrial complex II ar

54 steine residues are identified as sites of S-glutathionylation and found to be critical for redox-reg

55 We measured beta1 subunit glutathionylation and function of Na(+)-K(+)-ATPase in m

56 sistent with the fact that PABA/NO induces S-glutathionylation and inactivation of PTP1B, one phospha

57 tions were due, in large part, to reversible glutathionylation and inhibition of the Krebs cycle enzy

58 first enzyme identified to regulate UCP3 by glutathionylation and is the first study on the role of

59 ow evidence for the molecular basis of the S-glutathionylation and its structural impact on channel g

60 d search for protein modifications, cysteine glutathionylation and O-linked glycosylation featured pr

61 increased levels of GSNO caused increased S-glutathionylation and partial dimerization of hBCATc, su

62 Glutathionylation and phosphorylation of SOD1 is omnipre

63 eficiency in endothelial cells promoted eNOS glutathionylation and reduced its enzymatic activity, wh

64 lization of the protein S-thiolation forms S-glutathionylation and S-cysteinylation in response to in

65 ase function and 3 Ox-PTM: disulfide bond, S-glutathionylation and S-nitrosation were assessed.

66 O(2)(.-), only XOR inhibition reduced eNOS S-glutathionylation and Ser-1177 phosphorylation and resto

67 eNOS S-glutathionylation and Ser-1177 phosphorylation were sign

68 show that monocyte priming results in the S-glutathionylation and subsequent inactivation and degrad

69 ty is influenced in a reversible manner by S-glutathionylation and suggest that cellular GSH may regu

70 in completely resistant to inactivation by S-glutathionylation, and a mutant expressing this mutation

71 Cys(43) had only a modest contribution to S-glutathionylation, and Cys(120) was modulated by extrace

72 ave been described, including sulfenylation, glutathionylation, and disulfide formation.

73 susceptible to reversible S-nitrosylation, S-glutathionylation, and disulfide oxidation.

74 c mechanism for inhibition of BAK1 by C408 S-glutathionylation, and more generally, support the notio

75 to shift the poise toward E2 species reduced glutathionylation, and ouabain eliminated a ONOO(-)-indu

76 rent redox modifications (S-nitrosylation, S-glutathionylation, and oxidation to disulfides).

77 Cysteine targets for S-palmitoylation, S-glutathionylation, and S-nitrosylation show little corre

78 use post-translational modifications such as glutathionylation are often induced by oxidative stress,

79 ally, support the notion of protein kinase S-glutathionylation as a means of redox signaling in plant

80 lar, we have identified irreversible protein glutathionylation as a process associated with cellular

81 vidence supports the importance of protein S-glutathionylation as a regulatory post-translational mod

82 d, we identified increased endothelial NOS s-glutathionylation as the main mechanism for NOS uncoupli

83 H2O2 induces reversible S-glutathionylation at conserved cysteine residues within

84 thione leads to TRPC5 activation via TRPC5 S-glutathionylation at Cys176/Cys178 residues.

85 Catalysis of S-glutathionylation at low pK cysteines in proteins is a n

86 genes, was posttranslationally modified by S-glutathionylation at this conserved cysteine residue and

87 s actin deglutathionylation, increased actin glutathionylation, attenuated actin polymerization, and

88 ulatory cysteines made them inaccessible for glutathionylation but had no profound effect on the enzy

89 vel findings indicate that increased TRPC5 S-glutathionylation by oxidative stress and decreased TRPC

90 ective and versatile approach to identifying glutathionylation by using a mutant of glutathione synth

91 These effects were reversed using diamide, a glutathionylation catalyst.

92 antiproliferative activity and extents of S-glutathionylation correlated well with levels of intrace

93 in fresh kidney slices, the increased AQP2 S-glutathionylation correlated with tert-butyl hydroperoxi

94 that a frequent GSTO1-1 polymorphism affects glutathionylation cycle reactions reveals a common mecha

95 rase GSTO1-1 plays a significant role in the glutathionylation cycle.

96 Similar to sulfenylation, we observe glutathionylation decouples BiP ATPase and peptide bindi

97 We have examined whether glutathionylation depends on the conformational changes

98 that susceptibility of the beta1 subunit to glutathionylation depends on the conformational poise of

99 Susceptibility of the beta1 subunit to glutathionylation depends on the conformational poise of

100 low methods demonstrated that although actin glutathionylation did not significantly alter the rate c

101 peroxide scavenger ebselen, reduced Sirt3 S-glutathionylation, diminished SOD2 acetylation, and redu

102 tion was associated with increased complex I glutathionylation diminishing its activity.

103 redox protein, is shown to rescue eNOS from glutathionylation during ischemia-reperfusion in a GSH-i

104 We show glutathionylation enhances cell proliferation during oxi

105 , thus confirming the protective effect of S-glutathionylation from the oxidative damage of nitration

106 nstrate the physiological relevance of the S-glutathionylation-GRX redox module in controlling the ma

107 Glutathionylation has emerged as a key modification requ

108 es of redox-state-dependent protein kinase S-glutathionylation have fueled discussion of redox-sensit

109 While investigating EGF-induced glutathionylation in A431 cells, paradoxically we found

110 ) leukocytes and up-regulated levels of eNOS glutathionylation in aortas of C57BL/6 mice.

111 er WT or mutant eNOS rendered resistant to S-glutathionylation in cells with Tet-regulated expression

112 Ouabain further reduced glutathionylation in E2 and eliminated an increase seen

113 We show that eNOS S-glutathionylation in endothelial cells, with loss of NO

114 r the first time that AQP2 is subjected to S-glutathionylation in kidney and in HEK-293 cells stably

115 ass spectrometry revealed that C91 undergoes glutathionylation in macrophages activated with the TLR4

116 Preventing MKP-1 S-glutathionylation in metabolically stressed monocytes by

117 ostasis in mice, and we identify basal TAZ S-glutathionylation in murine kidney lysates, which is ele

118 Signals for glutathionylation in Na(+)-K(+)-ATPase-enriched membrane

119 utaredoxin and ROS- induced reversible actin glutathionylation in regulation of actin dynamics in neu

120 SG formation and, consequently, ATP synthase glutathionylation in response to H(2)O(2) challenges.

121 Protein glutathionylation in response to oxidative stress can af

122 le posttranslational modification, namely, S-glutathionylation in stressed states, including DNA dama

123 trometry was used to identify the sites of S-glutathionylation in TH.

124 lation of potentially autoreactive PDC-E2 is glutathionylation, in which the lysine-lipoic acid moiet

125 Diabetes promotes the S-glutathionylation, inactivation and subsequent degradati

126 Furthermore, the extent of S-glutathionylation increased in response to oxidative str

127 iously published experimental evidence for S-glutathionylation induced deactivation of the Arabidopsi

128 To address a possible role for BH4 in S-glutathionylation-induced eNOS uncoupling, we expressed

129 he first evidence that BH4 deficiency- and S-glutathionylation-induced mechanisms of eNOS uncoupling,

130 Glutathionylation involves reversible protein cysteine m

131 ent a novel mechanism for peptide or protein glutathionylation involving a carbon-sulfur cross-link b

132 We conclude that Prx2 glutathionylation is a favorable reaction that can occur

133 Protein S-glutathionylation is a posttranslational modification th

134 S-Glutathionylation is a redox-dependent post-translationa

135 Protein S-glutathionylation is a reversible redox-dependent post-t

136 These results suggest that S-glutathionylation is an important mechanism for the vasc

137 Because protein glutathionylation is associated with redox regulation, o

138 We further demonstrate that TAZ S-glutathionylation is critical for reactive oxygen specie

139 In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium

140 However, whether or not UCP3 glutathionylation is mediated enzymatically has remained

141 The relationship between AQP2 and S-glutathionylation is of potential interest because react

142 ROS levels, we resolved to determine whether glutathionylation is required for UCP2 regulation of GSI

143 ues by disulfide formation with glutathione (glutathionylation) is a reversible posttranslational mod

144 GSTO1-1 resulted in a 50% reduction in total glutathionylation levels.

145 sed aconitase activity, thus indicating that glutathionylation may be an important means of modulatin

146 These results suggest that actin glutathionylation may play a limited but defined role in

147 We hypothesized that actin glutathionylation may play a role in the multifactorial

148 However, it is unknown how S-glutathionylation may regulate the elasticity of titin a

149 Ca(2+), i.e. enhanced CICR, and suggest that glutathionylation may represent a fundamental mechanism

150 ion model in vivo This study suggests that S-glutathionylation may represent a mechanism by which CDC

151 sed CFTR function by oxidative modification (glutathionylation) may now be explained by high concentr

152 inactivated hBCATm, neither S-nitrosation, S-glutathionylation, nor dimerization could be detected, s

153 tic islets, we demonstrate that induction of glutathionylation not only deactivates UCP2-mediated pro

154 of conformation-dependent beta1 pump subunit glutathionylation, not restricted subsarcolemmal diffusi

155 he ratio of GSH:GSSG decreased significant S-glutathionylation occurred (with a further loss of 20% B

156 harmacologically relevant dose of PABA/NO, S-glutathionylation occurs rapidly (<5 min) and is sustain

157 Post-translational S-glutathionylation occurs through the reversible addition

158 Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchan

159 H) to PRDX2 cysteine residues (i.e., protein glutathionylation) occurs before or during PRDX2 release

160 and GST pi harboring bound GSH, followed by glutathionylation of 1-Cys Prx and then formation of an

161 Rapid glutathionylation of 1-Cys Prx in the heterodimer is det

162 lutathione (GSSG), induce isoform-specific S-glutathionylation of 6-phosphofructo-2-kinase/fructose-2

163 However, S-glutathionylation of ACS2 and ACS6 proteins was not dete

164 hondria with hydrogen peroxide resulted in S-glutathionylation of added recombinant TK2.

165 Glutathionylation of alpha-ketoglutarate dehydrogenase c

166 Glutathionylation of alpha-ketoglutarate dehydrogenase p

167 S-glutathionylation of ATP synthase alpha subunit occurred

168 s throughout the BAK1 kinase domain, whereas glutathionylation of C353 in the N-lobe and C374 near th

169 We found that glutathionylation of C408 allosterically destabilizes th

170 Glutathionylation of C408 also has structural consequenc

171 ll, MAL is not disulfide-bonded and requires glutathionylation of C91 for signaling.

172 at this was associated with an increase in S-glutathionylation of cell proteins, particularly actin.

173 Glutathionylation of cellular proteins by incubating cel

174 induced substantially increased levels of S-glutathionylation of cellular proteins in comparison wit

175 nd that GSTO1-1 is associated with the rapid glutathionylation of cellular proteins when the cells ar

176 f reactive oxygen species, carbonylation and glutathionylation of cellular proteins, inhibition of IK

177 To gain further insights into protein S-glutathionylation of complex I, we used two peptides of

178 S-glutathionylation of cryptic cysteines greatly decreases

179 Furthermore, we demonstrate that S-glutathionylation of cryptic cysteines in titin mediates

180 ontent (Fas-SH) and resultant increases in S-glutathionylation of Cys294, leading to increases of sur

181 Glutathionylation of cysteine 46 of the beta1 subunit of

182 Numerous studies of S-glutathionylation of cysteine thiols indicate that this

183 141 at the dimer interface of p53 and showed glutathionylation of either residue would inhibit p53-DN

184 ndogenous TNT-active GSTs catalyse excessive glutathionylation of endogenous substrates, depleting gl

185 Thus, S-glutathionylation of eNOS is a pivotal switch providing

186 Here we show that S-glutathionylation of eNOS reversibly decreases NOS activ

187 We reveal that S-glutathionylation of eNOS, by exposure to either 1,3-bis

188 d (FasL)-induced apoptosis is augmented by S-glutathionylation of Fas (Fas-SSG), which can be reverse

189 versely, overexpression of Grx1 attenuates S-glutathionylation of Fas and partially protects against

190 stimulation with Fas ligand (FasL) induces S-glutathionylation of Fas at cysteine 294 independently o

191 These results suggest that S-glutathionylation of Fas within the lung epithelium enha

192 ased FasL-induced oxidative processing and S-glutathionylation of Fas, resulting in decreased death-i

193 d interactions between Fas-ERp57-GSTP1 and S-glutathionylation of Fas.

194 GRx also enhanced the rate of S-glutathionylation of glyceraldehyde-3-phosphate dehydrog

195 S-glutathionylation of IKK-beta Cys-179 is reversed by glu

196 centrations of NAC and mito-Q instead caused glutathionylation of IKKalpha, thereby inhibiting its ac

197 The glutathionylation of intracellular protein thiols can pr

198 Glutathionylation of intracellular proteins is an establ

199 an be similarly regulated through reversible glutathionylation of its two conserved cysteine residues

200 levels and high GSSG levels and significant glutathionylation of mitochondrial proteins as well as b

201 Glutathionylation of mitochondrial proteins is a major c

202 Metabolic stress promoted the S-glutathionylation of MKP-1, targeting MKP-1 for proteaso

203 ncreased myofilament response to Ca(2+) with glutathionylation of myosin binding protein C.

204 Lastly, biochemical studies showed that glutathionylation of native IP(3)R(1) is increased in ce

205 The results indicate that GRx-dependent S-glutathionylation of p65-NFkappaB is most likely respons

206 Thus, it appears that S-glutathionylation of PDI is an upstream signaling event

207 Circular dichroism confirmed that S-glutathionylation of PDI results in alterations in the a

208 was undetectable, PABA/NO treatment caused S-glutathionylation of PDI.

209 Reversible S-glutathionylation of proteins is a focal point of redox

210 S-Glutathionylation of proteins is critical to cellular st

211 -like glutaredoxin is to catalyze reversible glutathionylation of proteins with GSH in cellular redox

212 and in the case of 13 inducing cross-linking glutathionylation of proteins.

213 However, glutathionylation of Prx V, not known to bind to Srx, wa

214 ROS exerts its effect through glutathionylation of PTEN (phosphatase and tensin homolo

215 Furthermore, in vitro S-glutathionylation of purified SQR resulted in enhanced S

216 Glutathionylation of reactive cysteines represents an ox

217 st, facilitating GS-radical scavenging and S-glutathionylation of redox signal mediators, consistent

218 These findings identify S-glutathionylation of Rpn2 as a contributory mechanism fo

219 t, increased oxidative stress results in the glutathionylation of sarcomeric actin.

220 Regulatory S-glutathionylation of the alpha subunit was induced in ra

221 oxidative modification of AMPK, including S-glutathionylation of the AMPKalpha and AMPKbeta subunits

222 O(2)-treated HEK 293 cells, activation and S-glutathionylation of the AMPKalpha subunit were present

223 urrents might be accounted for by changes in glutathionylation of the beta1 Na(+)-K(+) pump subunit,

224 have explored the possible involvement of S-glutathionylation of the catalytic alpha subunit in redo

225 Our findings imply that regulatory S-glutathionylation of the catalytic subunit plays a key r

226 oxygen species, along with carbonylation and glutathionylation of the cellular proteins.

227 The enzyme inhibition concurred with S-glutathionylation of the Cys-454, -458, -459, and -244.

228 We recently demonstrated that S-glutathionylation of the death receptor Fas (Fas-SSG) am

229 quires glutaredoxin 2-dependent reversible S-glutathionylation of the NAD(+)-dependent protein deacet

230 data indicate a physiological mechanism for glutathionylation of the oxidized catalytic cysteine of

231 -cysPrx with GSH-saturated pi GST results in glutathionylation of the oxidized cysteine in 1-cysPrx f

232 actin polymerization regulated by reversible glutathionylation of the penultimate cysteine mediated b

233 ubunit) were extensively glutathionylated; S-glutathionylation of these proteins resulted in a substa

234 eatments with redox active drugs, relative S-glutathionylation of these serpins was higher in plasma

235 ons support a role of Grx6 in regulating the glutathionylation of thiols of endoplasmic reticulum/Gol

236 ddition of dithiothreitol, suggesting that S-glutathionylation of TK2 is reversible.

237 K2 activity and protein levels, as well as S-glutathionylation of TK2.

238 We also observed S-glutathionylation of Trx1 and localized that redox modif

239 in intracellular nitric oxide that caused S-glutathionylation of various proteins.

240 S-Glutathionylation on Cys-189 was responsible for the obs

241 S-Glutathionylation on Cys47 and Cys101 autoregulates GSTp

242 ding did not suggest a large impact of actin glutathionylation on the binding to myosin-S1.

243 BAK1), we investigated the consequences of S-glutathionylation on the equilibrium conformational ense

244 cies-regulated effects on polymerization and glutathionylation on the one hand and the Grx1-mediated

245 teine 199 to alanine), oxidation, such as by glutathionylation or internal disulfide bond formation,

246 s expressing T338C CFTR to CuCl2, but not by glutathionylation or nitrosylation of the thiol or by ox

247 We propose that uncoupling of eNOS by S-glutathionylation- or by BH4-dependent mechanisms exempl

248 the isolated SQR was subjected to in vitro S-glutathionylation, oxidative modification and impairment

249 The identification of novel targets of glutathionylation, particularly in the secretome where t

250 PTP1B is known to be regulated by oxidation, glutathionylation, phosphorylation, and SUMOlyation, and

251 Reversible glutathionylation plays a critical role in protecting pr

252 Reversible protein glutathionylation plays a key role in cellular regulatio

253 lutathione disulfide and increased protein-S-glutathionylation prior to cell injury, indicating that

254 ated with redox regulation, our finding that glutathionylation promotes SOD1 monomer formation suppor

255 Cysteine 111 glutathionylation promotes SOD1 monomer formation, a nec

256 anslational modification of SOD1, especially glutathionylation, promotes dimer dissociation.

257 Here the intrinsic protein S-glutathionylation (PrSSG) at the 70-kDa FAD-binding subu

258 Protein S-glutathionylation (PSSG) is a posttranslational modifica

259 Our findings suggest that NOS s-glutathionylation, rather than BH4 depletion, accounts f

260 Our results show that GSTpi potentiates S-glutathionylation reactions following oxidative and nitr

261 kinetics of both the deglutathionylation and glutathionylation reactions.

262 and it also mediates GS transfer (protein S-glutathionylation) reactions, where GS (*) serves as a s

263 e functional relationships between BH4 and S-glutathionylation remain unknown.

264 rotein disulfide isomerase and catalyst of S-glutathionylation, respectively, in the ER.

265 s to functional inactivation of caspase 8 by glutathionylation, resulting in necroptosis, which occur

266 -N124K) had a significant decrease in AQP2 S-glutathionylation secondary to reduced ROS levels and re

267 ass spectrometric analysis revealed that the glutathionylation site is Cys-374.

268 d 5 mol/mol, respectively, and at least four glutathionylation sites were identified in the GS-DSDO-t

269 lfide formation, S-nitrosylation (SNO) and S-glutathionylation (SSG), have been recognized for their

270 Recently, we showed that the glutathionylation state of uncoupling protein-3 (UCP3) m

271 l agents, such as diamide, to alter the UCP3 glutathionylation state.

272 Collectively, our findings indicate that the glutathionylation status of UCP2 contributes to the regu

273 Consistent with S-glutathionylation, streptavidin pull-down assays with bi

274 Simulation modeling of Kir6.1 S-glutathionylation suggested that after incorporation to

275 human APE1 as the critical residue for the S-glutathionylation that leads to reduced AP endonuclease

276 rsensitive (k(inact) = 559 M(-1) s(-1)) to S-glutathionylation (thiolation) promoted by the presence

277 not the homomeric Kir4.1 is subject to the S-glutathionylation thus suggests a novel Kir4.1-Kir5.1 ch

278 resistant to inhibition by both diamide and glutathionylation, thus implicating this as the oxidatio

279 Here we show that Kir5.1 also enables S-glutathionylation to the heteromeric channel.

280 These results link S-glutathionylation to vertebrate development and successf

281 This finding of a S-glutathionylation-to-S-cysteinylation switch in a condit

282 -transferase proteins and enhanced protein S-glutathionylation, uncovering a previously unexplored va

283 endogenous GRx1, which also promotes protein glutathionylation under hypoxic radical generating condi

284 Here, we demonstrated that S-glutathionylation was a modulation mechanism underlying

285 Increase in S-glutathionylation was associated with dose- and time-dep

286 h an antibody against glutathione, protein S-glutathionylation was enhanced in post-ischemic myocardi

287 S-Glutathionylation was followed by suppression of the Na,

288 Glutathionylation was reversed by glutaredoxin 1 (Grx1),

289 In addition, we showed that sustained S-glutathionylation was temporally concurrent with drug-in

290 To facilitate the study of protein S-glutathionylation, we developed a synthesis and purifica

291 Increased levels of endogenous TRPC5 S-glutathionylation were observed in the striatum in both

292 sulfhydryls that had undergone H2O2 mediated glutathionylation were specifically derivatized with N-e

293 ne with either disulfide bond formation or S-glutathionylation, which induces eNOS uncoupling.

294 ified the ACO1 protein to be a subject for S-glutathionylation, which is consistent with our in silic

295 duces ROS elevation and, subsequently, TAZ S-glutathionylation, which promotes TAZ-mediated target ge

296 e TM2 helix of Kir5.1 was critical for the S-glutathionylation, which was accessible to intracellular

297 Reversing NOS s-glutathionylation with dithiothreitol (100 mumol/L) comp

298 re superior substrates for GRx-facilitated S-glutathionylation with GS-radical.

299 ormational poise of the Na(+)-K(+) pump, and glutathionylation with the pump stabilized in conformati

300 residues via sequential sulfenylation and S-glutathionylation within EGFR and the non-receptor-tyros