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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
57 ate, no activity was observed with cysteine, dithiothreitol, 2-mercaptoethanol, and 3-mercaptopropion
59 nditions and results in hyper-sensitivity to dithiothreitol, a reductant, whereas diamide, an oxidant
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
66 s synergistically increased by the reductant dithiothreitol, an effect mirrored by a whiB7-dependent
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
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
81 nhibition was reversed by the reducing agent dithiothreitol and unaffected by 1H-[1,2,4]oxadiazolo[4,
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
87 ter boiling for 5 min, with and without 1 mM dithiothreitol, and transmetallation in 100% serum at 37
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
98 treatment with antioxidants (glutathione and dithiothreitol) blocked the formation of ROS, reversed t
101 f human PrxV at 1.45 A resolution that has a dithiothreitol bound in the active site with its diol mo
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
123 any metal and requires the presence of both dithiothreitol (DTT) and 4 equiv of Fe(II) for maximum a
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
128 nhibition was reversed by the reducing agent dithiothreitol (DTT) and the specific deglutathionylatio
130 nd their alkyl derivatives using a cell-free dithiothreitol (DTT) assay under simulated physiological
132 idative activity measurement is based on the dithiothreitol (DTT) assay, where, after being oxidized
138 aggregate formation partially reversible by dithiothreitol (DTT) but not to recovery of activity.
140 in nanoparticle stability when treated with dithiothreitol (DTT) compared with monothiol analogues.
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
150 d, followed by chemical derivatization using dithiothreitol (DTT) of the phospho-serine/threonine-con
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
155 the treatment of purified portal rings with dithiothreitol (DTT) resulted in the disruption of the r
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
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
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
171 ides from the gold nanoparticle surface with dithiothreitol (DTT), which simplifies the assay and inc
183 ys were mimicked by the thiol-reducing agent dithiothreitol (DTT, 10 mm) and inhibited by the oxidizi
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
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
192 rK, and reduction of the oxidized protein by dithiothreitol fully restores DNA binding, indicating th
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
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
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
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
221 ta for online disulfide bond reduction using dithiothreitol on oxidized glutathione and insulin show
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
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
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
237 ilable-selenocystamine (catalyst precursor), dithiothreitol or tris(2-carboxyethyl)phosphine (reducta
239 2)-inactivated phosphorylated HMM or S1 with dithiothreitol partially reactivated the ATPase but had
241 Upon reduction of the disulfide bond by dithiothreitol, Pex5 transitioned to a noncovalent dimer
244 xpressing the W441C/K269C double mutant with dithiothreitol, radioactive transport was stimulated >2-
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
250 ter methanol denaturation and precipitation, dithiothreitol reduction, and iodoacetamide alkylation.
252 based on GalNAz-biotin labeling followed by dithiothreitol replacement and light chromatography/tand
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
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
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
272 ein was altered by addition of the reductant dithiothreitol, suggesting that the disulfide is importa
276 inactivation was reversed by the addition of dithiothreitol to microsomes isolated from treated RPTC.
278 molecule (RSH) such as GSH, thioredoxin, and dithiothreitol to produce a disulfide-S-monoxide (Prx-Cy
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
285 de treatment of Ku and could be abrogated by dithiothreitol treatment, demonstrating a reversible red
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
295 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)
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