ライフサイエンスコーパス: dithiothreitol

1 Xpert EBOV assay for semen samples by adding 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 c acid or after reduction of DHAA into AA by dithiothreitol.

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

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

8 f both reduced RNase and the model substrate dithiothreitol.

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

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

11 h effects were reversible by the addition of dithiothreitol.

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

13 by global effectors such as tunicamycin and dithiothreitol.

14 nsable for the oxidation of reduced RNase or dithiothreitol.

15 nted by antioxidants and the reducing agent, dithiothreitol.

16 uding glutathione, beta-mercaptoethanol, and dithiothreitol.

17 sed by the application of the reducing agent dithiothreitol.

18 d be recovered upon disulfide reduction with dithiothreitol.

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

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

21 d reduced RNase and with the model substrate dithiothreitol.

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

23 reticulum stress, including tunicamycin and dithiothreitol.

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

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

26 utant by disrupting the disulfide bonds with dithiothreitol.

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

28 pon disulfide reduction of the proteins with dithiothreitol.

29 activity is stimulated by both detergent and dithiothreitol.

30 , but activity is enhanced by treatment with dithiothreitol.

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

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

33 ells were treated with the ER stress inducer dithiothreitol.

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

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

36 ition was found with beta-mercaptoethanol or dithiothreitol.

37 The blocked currents were restored by 10 mm dithiothreitol.

38 was largely irreversible on incubation with dithiothreitol.

39 process between dansyl-linked disulfides and dithiothreitol.

40 ort is inhibited by the thiol reducing agent dithiothreitol.

41 Inhibition was reversible with dithiothreitol.

42 spectrometry in the absence and presence of dithiothreitol.

43 but activity was restored after addition of dithiothreitol.

44 ATP-evoked currents prior to reduction with dithiothreitol.

45 ed DksA on transcription are reversible with dithiothreitol.

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

47 TRPA1 activation, as did the reducing agent dithiothreitol.

48 ich was partially restored by treatment with dithiothreitol.

49 ed after reduction of intact antibodies with dithiothreitol.

50 goes dramatic activation upon reduction with dithiothreitol.

51 e PGE2 synthesis activity in the presence of dithiothreitol.

52 ited heme oxidation by H2O2 and reduction by dithiothreitol.

53 conductance response, an effect reversed by dithiothreitol.

54 to ER stress agents such as tunicamycin and 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 Maximal inhibition for ZnCl(2) and L-dithiothreitol (2a) corresponded to Zn(2):L-DTT stoichio

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

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

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

62 oprotein that binds FAD tightly and oxidizes dithiothreitol about 1000-fold slower than intact QSOX.

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

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

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

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

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

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

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

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

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

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

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 mmunized with C. albicans cells treated with dithiothreitol and protease (YDP cells), which exposed G

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 he presence of excess amounts of cysteine or dithiothreitol blocks this inhibition of binding.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 g disulfide bond-reducing molecules, such as dithiothreitol (DTT) and mercaptoethanol (ME), as releas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 Dithiothreitol (DTT) is the standard reagent for reducin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 affinity cleavage reagent in the presence of dithiothreitol/H(2)O(2).

195 limination followed by Michael addition with dithiothreitol has significantly improved the site mappi

196 235, is also a free thiol in the presence of dithiothreitol; however, in the absence of reductant, Cy

197 2)-treated mitochondria was reactivated with dithiothreitol, implicating oxidation of a protein sulfh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 Dithiothreitol inhibited formation of the beta-tubulin/d

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

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

215 When dithiothreitol is removed from purified single Cys mutan

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

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

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

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

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

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

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

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

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

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

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

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

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

229 Dithiothreitol or glutathione-reduced ethyl ester signif

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

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

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

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

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

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

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

237 ilable-selenocystamine (catalyst precursor), dithiothreitol or tris(2-carboxyethyl)phosphine (reducta

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

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

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

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

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

243 However, dithiothreitol prevents and reverses these effects on TH

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

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

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

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

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

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

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

251 , which were reverted to an inactive form by dithiothreitol reduction.

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

253 goes inactivation; subsequent treatment with dithiothreitol restores activity.

254 Addition of dithiothreitol resulted in complete conversion from full

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

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

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

258 Dithiothreitol reversed SNCEE-induced S-nitrosylation, A

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 Reduction of the native mucin with dithiothreitol, thereby breaking the S==S bonds between

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

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

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

279 Addition of dithiothreitol to the reaction mixture reversed the conv

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

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

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

283 47C) was locked in a low affinity state, and dithiothreitol treatment restored the capability of bein

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

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

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

287 t to activation but became activatable after dithiothreitol treatment.

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

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

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

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

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

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

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

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

296 Addition of the reducing agent dithiothreitol was unable to compensate for the lack of

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)