ライフサイエンスコーパス: dithiothreitol

1 to ER stress agents such as tunicamycin and dithiothreitol.

2 ic enzymes were conducted in the presence of dithiothreitol.

3 to DNA and lost activity in the presence of dithiothreitol.

4 site binding (four sites) in the presence of dithiothreitol.

5 g the in vitro oxidation of reduced RNase or dithiothreitol.

6 in and HIV-1 Tat, but not to thapsigargin or dithiothreitol.

7 f both reduced RNase and the model substrate dithiothreitol.

8 ese two agonists, but not to thapsigargin or dithiothreitol.

9 mutated [Fe]-hydrogenase in the presence of dithiothreitol.

10 h effects were reversible by the addition of dithiothreitol.

11 o air and reconstituted by treatment with dl-dithiothreitol.

12 by global effectors such as tunicamycin and dithiothreitol.

13 nsable for the oxidation of reduced RNase or dithiothreitol.

14 Xpert EBOV assay for semen samples by adding dithiothreitol.

15 nted by antioxidants and the reducing agent, dithiothreitol.

16 uding glutathione, beta-mercaptoethanol, and dithiothreitol.

17 d be recovered upon disulfide reduction with dithiothreitol.

18 d in the presence of reducing agents such as dithiothreitol.

19 disulfide cross-link by incubation with 1 mm dithiothreitol.

20 d reduced RNase and with the model substrate dithiothreitol.

21 es, an effect reversed by the reducing agent dithiothreitol.

22 etic, Tiron, or by treating homogenates with dithiothreitol.

23 tivities of H17'C and R19'C were reversed by dithiothreitol.

24 utant by disrupting the disulfide bonds with dithiothreitol.

25 ence of manumycin A that could be blocked by dithiothreitol.

26 pon disulfide reduction of the proteins with dithiothreitol.

27 activity is stimulated by both detergent and dithiothreitol.

28 , but activity is enhanced by treatment with dithiothreitol.

29 Fuc conjugates in the presence of Mn(2+) and dithiothreitol.

30 ases that are activated in vitro by iron and dithiothreitol.

31 o DNA binding activity, which is reversed by dithiothreitol.

32 is 84-95% and can be completely reversed by dithiothreitol.

33 ition was found with beta-mercaptoethanol or dithiothreitol.

34 The blocked currents were restored by 10 mm dithiothreitol.

35 was largely irreversible on incubation with dithiothreitol.

36 c acid or after reduction of DHAA into AA by dithiothreitol.

37 process between dansyl-linked disulfides and dithiothreitol.

38 ort is inhibited by the thiol reducing agent dithiothreitol.

39 Inhibition was reversible with dithiothreitol.

40 sed by the application of the reducing agent dithiothreitol.

41 reticulum stress, including tunicamycin and dithiothreitol.

42 ns via the cleavage of the disulfide bond by dithiothreitol.

43 ells were treated with the ER stress inducer dithiothreitol.

44 but activity was restored after addition of dithiothreitol.

45 ATP-evoked currents prior to reduction with dithiothreitol.

46 ed DksA on transcription are reversible with dithiothreitol.

47 its activity was almost 4-fold stimulated by dithiothreitol.

48 TRPA1 activation, as did the reducing agent dithiothreitol.

49 ich was partially restored by treatment with dithiothreitol.

50 ed after reduction of intact antibodies with dithiothreitol.

51 goes dramatic activation upon reduction with dithiothreitol.

52 e PGE2 synthesis activity in the presence of dithiothreitol.

53 ited heme oxidation by H2O2 and reduction by dithiothreitol.

54 conductance response, an effect reversed by dithiothreitol.

55 doacetamide-labeled Ras that was reversed by dithiothreitol (10 mmol/L), indicating a decrease in the

56 Reversing NOS s-glutathionylation with dithiothreitol (100 mumol/L) completely restored NOS act

57 ate, no activity was observed with cysteine, dithiothreitol, 2-mercaptoethanol, and 3-mercaptopropion

58 nditions and results in hyper-sensitivity to dithiothreitol, a reductant, whereas diamide, an oxidant

59 In the presence of dithiothreitol, a total reactivation of the inhibited ur

60 The reductant, dithiothreitol, abolished the effects of H2O2, suggestin

61 d by an increase in the absorption of the Co-dithiothreitol adduct, elicited by adding ca. 3 mol equi

62 that binds Zn(2+) relatively weakly (unlike dithiothreitol), allows rapid inhibition of oxidase acti

63 However, reduction by dithiothreitol (an artificial reducing compound) induced

64 s synergistically increased by the reductant dithiothreitol, an effect mirrored by a whiB7-dependent

65 We found that reducing agents (dithiothreitol and 2,3-dimercapto-1-propanesulfonic acid

66 tates displays reactivity toward thiols like dithiothreitol and 2-mercaptoethanol as well as reagents

67 a model, we reduced the disulfide bonds with dithiothreitol and alkylated the free sulfhydryl groups

68 sured using antioxidant surrogates including dithiothreitol and ascorbic acid, assuming that the deca

69 ly added to NOS enzyme preparations, such as dithiothreitol and beta-mercaptoethanol, probably preser

70 for the wild-type enzyme in the presence of dithiothreitol and for the IDH1/IDH2(C150S) enzyme in th

71 for isocitrate (two sites) in the absence of dithiothreitol and full-site binding (four sites) in the

72 found that exposure to OP measured using the dithiothreitol and glutathione assays drives higher risk

73 s sensitive to pH, catalase, and reductants (dithiothreitol and glutathione), consistent with oxidati

74 ally protected from reducing agents, such as dithiothreitol and glutathione, was conducted.

75 ing potential in the presence and absence of dithiothreitol and Mg2+.

76 Both forms of roGFP can be reduced with dithiothreitol and oxidized with hydrogen peroxide.

77 Dithiothreitol and P3001 were directly compared with NAC

78 ieved full MCR activation in the presence of dithiothreitol and protein components A2, an ATP carrier

79 Likewise, the antioxidants dithiothreitol and tempol did not reverse permeabilizati

80 binding was observed only in the presence of dithiothreitol and thus is redox-sensitive.

81 nhibition was reversed by the reducing agent dithiothreitol and unaffected by 1H-[1,2,4]oxadiazolo[4,

82 g the oocytes to a competing thiol like DTT (dithiothreitol) and 2-ME (2-mercaptoethanol).

83 endoplasmic reticulum caused by tunicamycin, dithiothreitol, and azole-class antifungal drugs can ind

84 reaction of the thiol groups of glutathione, dithiothreitol, and hemoglobin with maleimide-PEG have b

85 h ER stress inducers including thapsigargin, dithiothreitol, and NGI-1.

86 sses the ER stress response caused by virus, dithiothreitol, and thapsigargin as measured by global p

87 eticulum (ER) stress, including brefeldin-A, dithiothreitol, and thapsigargin.

88 ter boiling for 5 min, with and without 1 mM dithiothreitol, and transmetallation in 100% serum at 37

89 Binding of exogenous ligands (GSH, dithiothreitol, and tris-(2-carboxyethyl)-phosphine) to

90 itivity by >50% but increased sensitivity to dithiothreitol approximately 3-fold.

91 ies of these enzymes have generally employed dithiothreitol as a cosubstrate to reductively cleave th

92 t the usual trypsin digestion protocol using dithiothreitol as the reducing agent in ammonium bicarbo

93 s with strong resistance to competition from dithiothreitol (as high as 1.5 M) have also been prepare

94 idative activity measurement is based on the dithiothreitol assay (DTT assay), uses colorimetric dete

95 mon OP measurement techniques, including the dithiothreitol assay, glutathione assay, and ascorbic ac

96 f water-insoluble and water-soluble OP(DTT) (dithiothreitol assay, measure of oxidative potential per

97 he uric acid, ascorbic acid, glutathione, or dithiothreitol assays.

98 imination, followed by Michael addition with dithiothreitol (BEMAD).

99 In cultured hepatocytes, L-NAME or dithiothreitol blocked cholate-induced down-regulation o

100 treatment with antioxidants (glutathione and dithiothreitol) blocked the formation of ROS, reversed t

101 to the DNA, and this binding was reversed by dithiothreitol both in vitro and in vivo.

102 f human PrxV at 1.45 A resolution that has a dithiothreitol bound in the active site with its diol mo

103 ed as an FAD-containing protein reducible by dithiothreitol but not by NAD(P)H.

104 ve toward reduced ribonuclease A (RNase) and dithiothreitol but shows a >100-fold lower k cat/ K m fo

105 of ferrous iron in the presence of IscS and dithiothreitol but without L-cysteine, nearly all iron i

106 he plasma membrane, diminished the effect of dithiothreitol, but had no effect on inside-out signalin

107 that mycothiol, like reduced thioredoxin and dithiothreitol, can reduce oxidized RsrA to activate its

108 (disulfide)s and their depolymerization with dithiothreitol causes the appearance and disappearance o

109 lues) by use of antioxidants (ascorbic acid, dithiothreitol, citric acid) and can be accounted for in

110 The dependence of agonist binding on the dithiothreitol concentration followed a monophasic curve

111 d from the protein matrix by incubation with dithiothreitol, confirming that the active metabolite is

112 thiolation and activation can be reversed by dithiothreitol, confirming the importance of a disulfide

113 decreases upon treatment with tunicamycin or dithiothreitol, consistent with increased levels of unfo

114 hiols by diethylmaleate or co-treatment with dithiothreitol decreased the accumulation of a biotinyla

115 The pseudo first order rate constant of dithiothreitol-dependent N-terminal cleavage is 1 x 10(-

116 contains two genes encoding NAD+, Mn2+, and dithiothreitol-dependent phospho-alpha-glucosidases that

117 ulfide exchange of dansyl groups mediated by dithiothreitol depends on the structure of the dendrimer

118 oxidative potential (OP(GSH) and OP(AA)) and dithiothreitol depletion (OP(DTT)).

119 ce of SAM or an analogue and the presence of dithiothreitol, dihydrolipoate, or cysteine as ligands t

120 ivalent cation Mn(2+) and the reducing agent dithiothreitol directly shift integrins from their inact

121 h N-ethylmaleimide (thiol alkylating agent), dithiothreitol (disulfide reducing agent) was not able t

122 of warfarin resistance using the "classical" dithiothreitol-driven vitamin K 2,3-epoxide reductase (V

123 In contrast to results from the dithiothreitol-driven VKOR assay, all mutations exhibite

124 A semi-automated dithiothreitol (DTT) analytical system was used to measu

125 any metal and requires the presence of both dithiothreitol (DTT) and 4 equiv of Fe(II) for maximum a

126 With postcolumn introduction of dithiothreitol (DTT) and ammonium hydroxide, each disulf

127 to release the free drug was verified using dithiothreitol (DTT) and glutathione (GSH) as liberating

128 e residues using stable isotopic variants of dithiothreitol (DTT) and MS analysis.

129 nhibition was reversed by the reducing agent dithiothreitol (DTT) and the specific deglutathionylatio

130 The relative efficacy of dithiothreitol (DTT) and tris(2-carboxyethyl)phosphine (

131 soot were systematically measured using the dithiothreitol (DTT) assay (OP(DTT)).

132 Using the dithiothreitol (DTT) assay as a measure of OP, a combina

133 nd their alkyl derivatives using a cell-free dithiothreitol (DTT) assay under simulated physiological

134 A dithiothreitol (DTT) assay was used to measure the ROS-g

135 tial of DMSe-derived SOA, as measured by the dithiothreitol (DTT) assay, suggested the presence of ox

136 idative activity measurement is based on the dithiothreitol (DTT) assay, where, after being oxidized

137 particulate matter (PM) was measured by the dithiothreitol (DTT) assay.

138 ed by ambient particulate matter (PM) in the dithiothreitol (DTT) assay.

139 raction of the particles was measured by the dithiothreitol (DTT) assay.

140 passenger car engine was examined using the dithiothreitol (DTT) assay.

141 he cell surface when cells were treated with dithiothreitol (DTT) but not Mn(2+).

142 aggregate formation partially reversible by dithiothreitol (DTT) but not to recovery of activity.

143 The observations that dithiols such as dithiothreitol (DTT) cleave the persulfide with approxim

144 in nanoparticle stability when treated with dithiothreitol (DTT) compared with monothiol analogues.

145 The sulfhydryls of dithiothreitol (DTT) compete with thiophosphates for bin

146 luble oxidative potential (OP) determined by dithiothreitol (DTT) consumption and intracellular react

147 of Hb was initiated using the reducing agent dithiothreitol (DTT) in an assay that allowed the time f

148 phine (TCEP) is a widely used substitute for dithiothreitol (DTT) in the reduction of disulfide bonds

149 e that the reducing environment generated by dithiothreitol (DTT) in vivo inhibited Pho induction in

150 Adding dithiothreitol (DTT) is the standard method for liquefac

151 Dithiothreitol (DTT) is the standard reagent for reducin

152 be the primary driver of HOOH production and dithiothreitol (DTT) loss in ambient PM extracts.

153 Sulfhydryl reduction by dithiothreitol (DTT) lowered VS(max) KCC flux in AA and

154 d, followed by chemical derivatization using dithiothreitol (DTT) of the phospho-serine/threonine-con

155 Dithiothreitol (DTT) or reduced glutathione (GSH) was re

156 volume of concentrated reducing agent, viz. dithiothreitol (DTT) or tris(2-carboxyethyl)phosphine (T

157 ALDI-MS: (i) insulin disulfide reductions in dithiothreitol (DTT) over a range of heater temperatures

158 rmation and have insignificant impact on the dithiothreitol (DTT) oxidase activity of ALR.

159 the treatment of purified portal rings with dithiothreitol (DTT) resulted in the disruption of the r

160 Conversely, the reducing agent dithiothreitol (DTT) selectively enhanced NMDAR response

161 Treatment of sera with dithiothreitol (DTT) showed that the majority of remaini

162 acetate and either dithioerythritol (DTE) or dithiothreitol (DTT) soaked into H-Ras-GppNHp crystals i

163 y, a (310)GSH-spiked sample was treated with dithiothreitol (DTT) to convert disulfide-bonded glutath

164 pe enzyme, seven Cs could be modified before dithiothreitol (DTT) treatment; nine Cs could be modifie

165 Dithiothreitol (DTT) was used in all solutions from the

166 y than 108V, whereas in the presence of 4 mm dithiothreitol (DTT) we found no significant differences

167 ammatory cells from the presence of residual dithiothreitol (DTT), a reagent that reduces cell viabil

168 We examined the effects of dithiothreitol (DTT), a reducing agent that causes the f

169 en labeled and unlabeled Fdx is catalyzed by dithiothreitol (DTT), a result that was confirmed by mas

170 fered at physiological pH in the presence of dithiothreitol (DTT), and shows typical half-times of eq

171 ompared the effects of three reducing agents-dithiothreitol (DTT), beta-mercaptoethanol (beta-MCE), a

172 ulation procedure relies on formaldehyde and dithiothreitol (DTT), but these active chemicals may int

173 urface-exposed dimers that were sensitive to dithiothreitol (DTT), dependent on the Mip domain and on

174 When assayed in the presence of dithiothreitol (DTT), the inhibitory effect was drastica

175 ides from the gold nanoparticle surface with dithiothreitol (DTT), which simplifies the assay and inc

176 ce on the kinetics of disulfide reduction by dithiothreitol (DTT).

177 oss-links, and that these are susceptible to dithiothreitol (DTT).

178 toward the oxidation of the model substrate dithiothreitol (DTT).

179 rming MTSEA is blocked by the reducing agent dithiothreitol (DTT).

180 c measurements in the presence or absence of dithiothreitol (DTT).

181 )beta, and this can be partially reversed by dithiothreitol (DTT).

182 mption in the presence of suspended NP's and dithiothreitol (DTT).

183 ic ion, and a molecule of the MerB inhibitor dithiothreitol (DTT).

184 ion only after exposure to a reducing agent, dithiothreitol (DTT).

185 alpha-Azido esters, when treated with dithiothreitol (DTT)/diisopropylethylamine (DIPEA), unde

186 Preincubation with the reducing agent dithiothreitol (DTT, 1 mM) prevented drug-induced inhibi

187 Pretreatment of IPAs with dithiothreitol (DTT, 1 mm), proposed to promote the conv

188 ys were mimicked by the thiol-reducing agent dithiothreitol (DTT, 10 mm) and inhibited by the oxidizi

189 The thiol reducing agent dithiothreitol (DTT, 5.0 mm) both prevented and reversed

190 oactive thiol reagent, 1-S-[3H]carboxymethyl-dithiothreitol (DTT-S-C[3H(2)]CO(2)H, [3H]CM-DTT), was d

191 separated from transketolase by SDS-PAGE (+/-dithiothreitol [DTT]) and identified by peptide sequenci

192 (4 M KCl, 0.05 M HEPES buffer, pH 7.5, 0.1% dithiothreitol [DTT]).

193 (pH 7.5), 0.5 M NaCl, 0.5% NP-40, and 10 mM dithiothreitol [DTT].

194 Isolated rods are stable in dithiothreitol, EGTA, Ca(2+), and ATP.

195 limination followed by Michael addition with dithiothreitol facilitates the study of the labile O-Glc

196 mide and the disulfide bonds were reduced by dithiothreitol followed by alkylation with radiolabeled

197 of alpha-chain-binding proteins by means of dithiothreitol following purification.

198 rK, and reduction of the oxidized protein by dithiothreitol fully restores DNA binding, indicating th

199 Dithiothreitol, glutathione and the C207A mutant of E. c

200 y genes were induced by oxidative stress and dithiothreitol in fibroblasts but not HeLa cells; conver

201 xamine cellular response to stress caused by dithiothreitol in HeLa cells, where we identified and qu

202 nzyme is activated by reaction with Fe2+ and dithiothreitol in the absence of air.

203 Replacing beta-mercaptoethanol with dithiothreitol in the loading buffer did not eliminate t

204 We found that 5 mm dithiothreitol in the purification process enhanced olig

205 poxic cells that were also treated with NAC, dithiothreitol increased p65-NFkappaB DNA binding.

206 more, bath application of the reducing agent dithiothreitol increased the NMDAR component of the syna

207 ly 20-fold in platelets, and both Mn(2+) and dithiothreitol increased the probability more than 2-fol

208 e as bath application of the reducing agent, dithiothreitol, increased the NMDAR component of the syn

209 ibutyl disulfide when PPIs were treated with dithiothreitol indicated occurrence of sulfhydryl-disulf

210 t of H(2)O(2) was reversed by treatment with dithiothreitol indicating that H(2)O(2) acts by promotin

211 ch was lost after treatment of the sera with dithiothreitol, indicating IgM antibody-mediated cytotox

212 d in both mutant proteins by incubation with dithiothreitol, indicating that the lack of cytotoxic ac

213 globular without visible stalks, Mn(2+) and dithiothreitol induced a significant increase in the pro

214 ic acid were found to reduce tunicamycin- or dithiothreitol-induced autophagy, but not autophagy caus

215 Dithiothreitol inhibited formation of the beta-tubulin/d

216 iron in the presence of IscS, L-cysteine and dithiothreitol, iron-sulfur clusters are assembled in Is

217 ly inhibit R2 RNR protein in the presence of dithiothreitol is likely related to Fe chelating propert

218 f the disulfide bond of the gamma subunit by dithiothreitol is not decreased by truncated epsilon, al

219 When dithiothreitol is removed from purified single Cys mutan

220 and NADP, and reduction of the crystals with dithiothreitol just prior to data collection.

221 cetylcysteine, or adding the reducing agent, dithiothreitol, lessened the response.

222 as repeated twice with the addition of 10 mM dithiothreitol, making a total of three extractions.

223 NO with selected thiols, including cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and

224 The sulfhydryl-reducing agent, dithiothreitol, normalized the sensitivity of KCC activa

225 tion was assessed by observing the effect of dithiothreitol on currents evoked by ATP.

226 ta for online disulfide bond reduction using dithiothreitol on oxidized glutathione and insulin show

227 The effects of NO, GSNO and dithiothreitol on sperm protein S-nitrosylation, assesse

228 ster [L-NAME]) or protein nitrosylation (via dithiothreitol) on bile salt homeostasis in male Wistar

229 tivated glutaredoxin could be reactivated by dithiothreitol only in the presence of urea, followed by

230 owever, lowering the concentration of either dithiothreitol or beta-mercaptoethanol eliminated the ba

231 ith precipitate should be incubated in 10 mM dithiothreitol or beta-mercaptoethanol until the precipi

232 and insulin was reversed upon reduction with dithiothreitol or by inhibiting NOS or PI3K.

233 with the existence of sodium L-ascorbate, DL-Dithiothreitol or cysteine.

234 Dithiothreitol or glutathione-reduced ethyl ester signif

235 tein response activation upon challenge with dithiothreitol or heat shock in our yeast model system.

236 cued in this mutant by growth with exogenous dithiothreitol or L-cysteine, suggesting that in the abs

237 Disruption of these disulfide bonds by dithiothreitol or mutation of the conserved cysteines re

238 be reversed by treatment with the reductants dithiothreitol or reduced glutathione or by incubation w

239 disulfide bonds because their reduction with dithiothreitol or substitution of Cys22 with alanine led

240 or N-acetyl-L-cysteine and fully reduced by dithiothreitol or the E. coli thioredoxin/thioredoxin re

241 Bath application of dithiothreitol or TPEN (N,N,N',N'-tetrakis(2-pyridylmeth

242 Thirdly, exposure to dithiothreitol or tunicamycin revealed no evidence for a

243 2)-inactivated phosphorylated HMM or S1 with dithiothreitol partially reactivated the ATPase but had

244 With the addition of dithiothreitol, peptides derivatized by selenium reagent

245 Upon reduction of the disulfide bond by dithiothreitol, Pex5 transitioned to a noncovalent dimer

246 Similar to RPTC, dithiothreitol prevented TBHP-induced ER-iPLA(2) inactiv

247 However, dithiothreitol prevents and reverses these effects on TH

248 xpressing the W441C/K269C double mutant with dithiothreitol, radioactive transport was stimulated >2-

249 Treatment with the antioxidant dithiothreitol reduced RyR-mediated SR Ca(2+) leak in pe

250 ne dinucleotide, reduced form) and DTTre (DL-dithiothreitol, reduced form) was confirmed by light abs

251 Four diverse electron donors, ascorbate, dithiothreitol, reduced glutathione, and NADH, were each

252 that BES is a time-dependent inactivator of dithiothreitol-reduced 2-KPCC, where the redox active cy

253 A newly developed assay indicated that dithiothreitol-reduced MM1854 could transfer electrons t

254 ter methanol denaturation and precipitation, dithiothreitol reduction, and iodoacetamide alkylation.

255 specific isolation is followed by subsequent dithiothreitol release of the isolated EVs for downstrea

256 based on GalNAz-biotin labeling followed by dithiothreitol replacement and light chromatography/tand

257 goes inactivation; subsequent treatment with dithiothreitol restores activity.

258 e alpha subunit catalyzed by glutaredoxin or dithiothreitol resulted in restoration of the Na,K-ATPas

259 al potential of chloride, but treatment with dithiothreitol resulted in transport currents with the s

260 i cells with the ER stressors tunicamycin or dithiothreitol resulted in up-regulation of the expressi

261 Dithiothreitol reversed SNCEE-induced S-nitrosylation, A

262 Glutathione and dithiothreitol reversed the effect of curcumin on TNF-in

263 Removal of cysteine-bound ebselen with dithiothreitol reversed the effects of the drug on the h

264 ysteine substitution mutant, Cx26V37C formed dithiothreitol-sensitive dimers.

265 cell walls by Sed1- and Ecm33-dependent and dithiothreitol-sensitive mechanisms that enhance Q-cell

266 ods, isolated from stressed neurons, contain dithiothreitol-sensitive multimeric forms of cofilin, pr

267 in this study we identified a unique 35-kDa, dithiothreitol-sensitive nuclease and showed that it was

268 this study, we identified two unique 28-kDa, dithiothreitol-sensitive nucleases and showed that they

269 surface expression, predominantly as stable, dithiothreitol-sensitive trimers, but no fusion activity

270 Thus, GSH and dithiothreitol showed weaker binding, with estimated KD

271 ased from the sandwiches after dissolving in dithiothreitol solution (DTT 0.8M).

272 and redox titration of CrCAH3 function with dithiothreitol suggested a possible redox regulation of

273 sitive to inhibition with the reducing agent dithiothreitol, suggesting that oxidative stress resulte

274 This was reversed by the addition of dithiothreitol, suggesting that S-glutathionylation of T

275 ein was altered by addition of the reductant dithiothreitol, suggesting that the disulfide is importa

276 The purified protease was inhibited by dithiothreitol, suggesting the presence of an essential

277 For the in vitro reaction driven by dithiothreitol, the 43-51 deletion mutation retained 85%

278 inactivation was reversed by the addition of dithiothreitol to microsomes isolated from treated RPTC.

279 o nearly wild-type levels by adding Msr plus dithiothreitol to msr strain extracts.

280 molecule (RSH) such as GSH, thioredoxin, and dithiothreitol to produce a disulfide-S-monoxide (Prx-Cy

281 Addition of dithiothreitol to the reaction mixture reversed the conv

282 Addition of the reducing agent dithiothreitol to wild-type cells had a similar effect,

283 Application of dithiothreitol, to reduce protein -SNO groups, rapidly r

284 fective in disulfide bond formation restores dithiothreitol tolerance and periplasmic cytochrome b as

285 47C) was locked in a low affinity state, and dithiothreitol treatment restored the capability of bein

286 Dithiothreitol treatment reversed the H(2)O(2) inhibitio

287 de treatment of Ku and could be abrogated by dithiothreitol treatment, demonstrating a reversible red

288 e to proteolysis; some of them withstand the dithiothreitol treatment.

289 s that required solubilization by (repeated) dithiothreitol treatment.

290 The ER stress inducers thapsigargin and dithiothreitol trigger production of the pro-inflammator

291 as reduced to benzo[a]pyrene-7,8-catechol by dithiothreitol under anaerobic conditions and then furth

292 re reduced to the corresponding catechols by dithiothreitol under anaerobic conditions and then furth

293 dox protein is functionally substituted with dithiothreitol, VKOR overexpression increased the fIX ca

294 When GSH or dithiothreitol was added to the chaperone during the rec

295 lphavbeta3 mutant by activating antibody and dithiothreitol was also impaired.

296 onse of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the EG

297 -3, which was reversed by the reducing agent dithiothreitol, whereas PAPA or DEA NONOate did not bloc

298 ynitrite scavenger, deferoxamine, but not by dithiothreitol, which triggers reduction of S-nitrosylat

299 ected for cytochrome c assembly by exogenous dithiothreitol, which was consistent with the cytochrome

300 esized at the micromole level by reaction of dithiothreitol with tritiated iodoacetic acid (I-C[3H(2)