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1 , and the calcium-activated calcium channel (diamides).
2 A1 increased cellular sensitivity to tBH and diamide.
3 FP-tagged TNFRs exposed to the thiol oxidant diamide.
4 tance to catechol, MHQ, 1,4-benzoquinone and diamide.
5 as examined using the thiol-specific oxidant diamide.
6 crosslinking of transmembrane cysteines with diamide.
7  e, and g within adenosyl cobyrinic acid a,c-diamide.
8 ells treated with the thiol-specific oxidant diamide.
9  hydrogen peroxide, menadione, paraquat, and diamide.
10 ene hydroperoxide, t-butyl hydroperoxide, or diamide.
11 lted in the production of cobyrinic acid a,c-diamide.
12  tolerance but dispensable for resistance to diamide.
13 tein is treated with strong oxidants such as diamide.
14 e to both H2O2 and the thiol-oxidizing agent diamide.
15 shock and the thiol-specific oxidizing agent diamide.
16 the formation of ox-hHSF1 in the presence of diamide.
17 y induced (70-fold) following treatment with diamide.
18 anothione disulfide following oxidation with diamide.
19 owth inhibition by the thiol-oxidizing agent diamide.
20 e inactivation of NFI by the oxidizing agent diamide.
21 ility to induce this activity on exposure to diamide.
22 formation of the intersubunit cross-links by diamide.
23 identical to that obtained in the absence of diamide.
24 the channel by the disulfide inducing agent, diamide.
25 by amidation to form Ni-sirohydrochlorin a,c-diamide.
26 s increased sensitivity to the thiol oxidant diamide.
27 cued by the addition of the chemical oxidant diamide.
28 rmeant bis-quaternary ammonium derivative of diamide.
29 C56S mutation was resistant to the effect of diamide.
30 nstrate increased resistance to both tBH and diamide.
31 amide, and expression of trxD was induced by diamide.
32 -step synthesis of phthalimides and phthalic diamides.
33 e to new mode of action compounds, including diamides.
34 ate two important properties of these simple diamides.
35                                 In contrast, diamide 1) activates the channel, 2) enhances [3H]ryanod
36 tive double Heck cyclizations of cyclohexene diamides 1 and 3 form contiguous quaternary stereocenter
37        Treatment with high concentrations of diamide (1 mm) resulted in an increase in the FRET signa
38 reatment of cells with low concentrations of diamide (1 mum) that was not sufficient to provoke TNFR
39  for example, N,N,N'N'-tetrahexylpropane-1,3-diamide (1), N,N'-dibutyl-N,N'-dimethyl-2-tetradecylprop
40 nd eliminated the necessity of preparing the diamide 13.
41 ibutyl-N,N'-dimethyl-2-tetradecylpropane-1,3-diamide (2), or N,N,N'N'-tetramethylpropane-1,3-diamide
42                      In situ imidazolate-4,5-diamide-2-olate linker generation leads to the formation
43 prepared zinc-deuteroporphyrin diamide (ZnMb(diamide), 3), which converts the charged groups to neutr
44  10 mm) and inhibited by the oxidizing agent diamide (30 mum).
45 abeled zinc porphyrin derivative (ZnMb((15)N-diamide), 4).
46 sporter mutants, Deltaatr1 and Deltaflr1, to diamide, 4-NQO, and cadmium.
47 sic internal aromatic amine of 3 to give the diamide 5.
48 mide (2), or N,N,N'N'-tetramethylpropane-1,3-diamide (6), are poorly organized for metal ion complexa
49                                              Diamide 7 was prepared, and the X-ray crystal structure
50 id 2a (MB05032) led to the identification of diamide 8 (MB06322), the first reported orally efficacio
51  tolerance to the oxidative stress caused by diamide (a drainer of metabolic NADPH) in the absence of
52 peroxide, whereas they are more sensitive to diamide, a disulfide bond-inducing agent.
53            These effects were reversed using diamide, a glutathionylation catalyst.
54                    Control studies involving diamide, a membrane-stiffening agent, suggest that the R
55 of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces b
56                               We showed that diamide, a reagent that promotes disulfide bond formatio
57 M containing 25 mM glucose were treated with diamide, a thiol oxidant, at a concentration that did no
58 ramide, whereas treatment of astrocytes with diamide, a thiol-depleting agent, alone caused degradati
59                               Treatment with diamide, a thiol-oxidizing agent, induced formation of d
60                                        These diamides act on the ryanodine receptor (RyR), a large en
61 and cell lysates containing Sav mutants with diamide affords up to >100 TON's and only a modest erosi
62  cells treated with diethyl maleate (DEM) or diamide, agents that deplete cellular thiols, had increa
63 ibited by pro-oxidants hydrogen peroxide and diamide, although these two pro-oxidants by themselves h
64                                  Neutral N3S diamide amine thiol chelators with no adjacent positive
65 perimental and DFT study of the reactions of diamide-amine supported titanium hydrazides with alkynes
66 e inducible by exposure of cells to H2O2 and diamide, among other oxidative stress eliciting compound
67 vity to dithiothreitol, a reductant, whereas diamide, an oxidant had no effect on the growth of the m
68 data are consistent with a model in which 1) diamide, an oxidizing agent, simultaneously produces an
69 hylmaleimide (NEM), an alkylating agent, and diamide, an oxidizing agent, were examined for effects o
70 UVEC) monolayers for 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decrea
71 age at the alpha-carbon position through the diamide and alpha-amidation pathways.
72                                              Diamide and amido-ester derivatives proved to be efficie
73                Thiol reactive agents such as diamide and cadmium induce zinc efflux by interfering wi
74                                              Diamide and dithiothreitol were reagents used respective
75 tion 199 was resistant to inhibition by both diamide and glutathionylation, thus implicating this as
76                                Although both diamide and H(2)O(2) have been used to impose oxidative
77 e stress elicited by the redox-active agents diamide and H(2)O(2).
78 ional residues upon exposure to pro-oxidants diamide and H2O2 Here we hypothesize that routine storag
79 d function by the action of oxidants such as diamide and hydrogen peroxide; however, prior DNA bindin
80  or the glutathione-specific oxidizing agent diamide and in whole newborn mouse eyes incubated in the
81            In contrast, the oxidizing agents diamide and menadione inhibited the development of hillo
82                                              Diamide and N-ethylmaleimide likewise inhibit the disloc
83  potential and/or free thiol status, such as diamide and N-ethylmaleimide.
84 erential sensitivity of their RNA binding to diamide and N-ethylmaleimide.
85  mutant was more sensitive to the effects of diamide and oxygen than the parent strain.
86  fluorescence and comparison to the oxidants diamide and phenylhydrazine revealed that oxidation does
87 vely) to serine rendered HSF1 insensitive to diamide and prevented its conversion to ox-HSF1.
88                      Treatment of PTP1B with diamide and reduced glutathione or with only glutathione
89    In the presence of a low concentration of diamide and reduced glutathione, the kinase was rapidly
90 rsine oxide (PheArs) is greater than that by diamide and t-butylhydroperoxide (TBH), yet the increase
91  was also induced by the GSH-oxidizing agent diamide and the GSH-conjugating agent N-ethylmaleimide,
92 ed sensitivity to the thiol-specific oxidant diamide and to the redox cycling compounds menadione and
93 es of extractants (organophosphorus ligands, diamides and N-heterocycles), with a focus on the separa
94 elial cells with the thiol-specific oxidant, diamide, and assessed activities of the UPP.
95      The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to det
96 tective during exposure to the thiol oxidant diamide, and expression of trxD was induced by diamide.
97 esulted in increased sensitivity to benomyl, diamide, and menadione, but not 4-NQO, cycloheximide, or
98 tment of mouse brain synaptosomes with H2O2, diamide, and sodium nitroprusside caused aggregation of
99  also produced 1-desmethylcobyrinic acid a,c-diamide, and strains that had neither cbiP nor cbiA synt
100 the present study, we examined the effect of diamide, and the model oxidant hydrogen peroxide (H(2)O(
101  partially inhibited by N-ethylmaleimide and diamide, and unaffected by arsenite.
102                                              Diamide appears to oxidize particular cysteine residues
103    In addition, single channels activated by diamide are further activated by the addition of NEM.
104 ortho- and para-benzoquinones which act like diamide as thiol-reactive electrophiles.
105 in vivo is reduced when cells are exposed to diamide, as shown by the enhanced stability of an SsrA-t
106 ious concentrations of glutathione (GSH) and diamide at 25 degrees C for 1 hour.
107                                              Diamide at concentrations of up to 5 mM reduced the axia
108 iolation, we used the thiol-specific oxidant diamide because its oxidant activity is restricted to in
109 the double mutant R91C/G98D was resistant to diamide block.
110 ar proteins also shows that sulforaphane and diamide, both known to react with cysteine amino acids,
111 ese mutant factors confer hyperresistance to diamide but hypersensitivity to H(2)O(2).
112 bsence of ATP or adenosyl cobyrinic acid a,c-diamide, but the rate of glutamine hydrolysis is enhance
113                        Moreover, the oxidant diamide can restore growth and secretion in ero1 mutants
114 to thiol-specific stress conditions, such as diamide, catechol and 2-methylhydroquinone (MHQ).
115                                              Diamide caused a rapid increase in oxidized glutathione
116 cordings and inside-out patches, H(2)O(2) or diamide caused a strong inhibition of the vascular K(ATP
117      Oxidation of GSH with the thiol oxidant diamide caused significant decreases in cellular GSH and
118 kinase inhibitor to increase deformability), diamide (cell-stiffening agent), cilostazol (phosphodies
119 ning approach and identified a benzimidazole diamide compound designated GSK669 that selectively inhi
120   Of critical importance, a cyclic tartronic diamide coordinates the MetAP-2 metal ion in the active
121              Oxidizing agents, in particular diamide, could further enhance transcription of the trxB
122                When incubated with oxygen or diamide, CprK undergoes inactivation; subsequent treatme
123 d ATP release (111.7 +/- 17.2%) in older and diamide decreased RBC deformability (RCTT: 8.955 +/- 0.1
124                            The corresponding diamide derivative was also synthesized and analyzed fro
125      These results imply that the diester or diamide derivatives of the d-tetrapeptides self-assemble
126                                   Phosphonic diamides derived from amino acid esters were discovered
127 ation of a novel benzylpiperazine adamantane diamide-derived compound that inhibits EboV infection.
128  by thiol-ene addition copolymerization with diamide diene monomers.
129                        Notably, H(2)O(2) and diamide differentially affected the RyR2-FKBP12.6 intera
130                                            A diamide diimine ligand, [{-CH=N(1,2-C6H4)NH(2,6-iPr2C6H3
131           Moreover, in both HAECs and BAECs, diamide dramatically increased both the rate and magnitu
132  When examined for promoters up-regulated by diamide, effective Pap1 binding to these targets require
133                                          All diamide effects can be reversed by the reducing agent, d
134                                              Diamide either cross-links phase 1 sulfhydryls or causes
135 l modification by N-ethylmaleimide (NEM) and diamide, even under conditions that led to severe cellul
136 tionally, miRNAs are involved in response to diamide exposure, indicating they are probably associate
137 atment with the sulfhydryl oxidizing reagent diamide formed the faster migrating, slower dissociating
138 dly washed it away, and resumed culturing in diamide-free medium (post-diamide stress culturing).
139 TP-dependent synthesis of cobyrinic acid a,c-diamide from cobyrinic acid using either glutamine or am
140 nsformations to afford a wide variety of 1,2-diamide functionalized products.
141  phosphotyrosine residue, and a diester or a diamide group, we find that, regardless of the stereoche
142      Loss of TH catalytic activity caused by diamide-GSH is partially recovered by DTT and glutaredox
143                                The effect of diamide-GSH on TH activity is prevented by dithiothreito
144  were inhibited strongly by a combination of diamide/GSH or H(2)O(2)/GSH but not by either alone.
145 e in binding strength between the urea and a diamide guest in 0.1 M NBu4B(C6F5)4/CH2Cl2.
146                                   Similar to diamide, H(2)O(2) increased the sensitivity of HAECs to
147                                              Diamide had no effect on the C150S mutant enzyme, sugges
148 s and treated with three oxidative reagents (diamide, hydrogen peroxide, and phenylhydrazine) to cros
149 ns but can be oxidized by the strong oxidant diamide, implying that the redox potential for the thiol
150 mine, is inhibited by the sulfhydryl oxidant diamide in a concentration-dependent manner.
151 loss of sensitivity to both sulforaphane and diamide in electrophoretic mobility shift assay analysis
152                         Treatment of TH with diamide in the presence of [(35)S]GSH results in the inc
153 ance to two different oxidants, H(2)O(2) and diamide, in cells that contain an intact glutamate catab
154           Likewise, GSH markedly potentiated diamide inactivation of a PKC isozyme mixture purified f
155                                              Diamide inactivation of cPKC-alpha and its potentiation
156 the heme diester or, for the first time, the diamide increases the second-order rate constant of the
157 train produced 1-desmethylcobyrinic acid a,c-diamide, indicating that CbiD is involved in C-1 methyla
158 I, only 1-nitrosocyclohexalycetate (NCA) and diamide induced reproducible protein phosphorylation.
159 cetyl cysteine attenuated GSSG elevation and diamide-induced apoptosis.
160                                              Diamide-induced blocking was reversed by disulfide bond-
161                          GSH potentiation of diamide-induced cPKC-alpha inactivation was associated w
162          We describe a Pap1-Oxs1 pathway for diamide-induced disulfide stress in Schizosaccharomyces
163                                              Diamide-induced expression of trxC, trxE, and trxF incre
164                                              Diamide-induced formation of the Cys-150 disulfide bond
165                                              Diamide induces intersubunit dimer formation of both the
166 reincubation of the latent HSF1 monomer with diamide inhibited the in vitro heat-induced activation a
167 thermore, oxidizing agents, such as H2O2 and diamide, inhibited Gag processing of wild-type virions,
168 vidence that the G4946E RyR mutation impairs diamide insecticide binding.
169 dine receptor (RyR) was highly correlated to diamide insecticide resistance in field populations of P
170 cation enzymes have been associated with the diamide insecticide resistance in the diamondback moth,
171              Recently acquired resistance to diamide insecticides in this species is thought to be du
172                                              Diamide insecticides target insect ryanodine receptors (
173 gs elucidate the mode of action of different diamide insecticides, reveal the molecular mechanism of
174         The recent introduction of synthetic diamide insecticides, with a novel mode of action, poten
175              Calcium pulstrodes based on the diamide ionophore AU-1 were characterized and applied to
176                                              Diamide is a chemical oxidant that selectively converts
177 to treatment with the thiol-specific oxidant diamide is the result of transcription initiation at the
178 r conditions in which cAPK is inactivated by diamide, it is also readily thiolated.
179 III alkyl complexes supported by a ferrocene diamide ligand (1,1'-fc(NSi(t)BuMe(2))(2)) have been fou
180 -sandwich complexes supported by a ferrocene diamide ligand (NN(fc)) are reported.
181                  Utilizing a rigid ferrocene diamide ligand (NN(TBS)), a Dy(III) SIM, (NN(TBS))DyI(TH
182 a) benzyl complexes supported by a ferrocene diamide ligand are reactive toward aromatic N-heterocycl
183 yridyl complex supported by a 1,1'-ferrocene diamide ligand is reported.
184 nzyl complexes supported by a ferrocene 1,1'-diamide ligand.
185 benzyl complex supported by a ferrocene 1,1'-diamide ligand.
186 t, thus demonstrating the potential of rigid diamide ligands in the design of new SIMs with defined m
187                 Inhibition of TNF-alpha- and diamide-mediated depletion of GSH, elevation of ceramide
188 of Deltayap1 cells to the oxidants H(2)O(2), diamide, menadione and tert-butyl hydroperoxide.
189 rial libraries of dimeric iminodiacetic acid diamides, novel small molecule binders of EPOr were iden
190     Mitochondrial dysfunction in response to diamide occurred in stages, progressing from oscillation
191 um(0) and the chiral ligand derived from the diamide of trans-1,2-diaminocyclohexane and 2-diphenylph
192 sm, we report the semisynthesis of mono- and diamides of biliverdin IXalpha and those of its non-natu
193  were rapidly linked through oxidation (with diamide) of the Cys 73 disulfide bond, and the relative
194 itroxyl donors and the thiol-oxidizing agent diamide on cardiac myocyte protein phosphorylation and o
195                     The inhibitory effect of diamide on TH catalytic activity is enhanced significant
196 ap1 form a complex when cells are exposed to diamide or Cd that causes disulfide stress.
197 cellular Ca(2+), acute treatment with either diamide or H(2)O(2) increased the number of BAECs exhibi
198 xB gene was induced following treatment with diamide or H(2)O(2) or exposure to oxygen.
199 he same high level in the presence of either diamide or H(2)O(2), these mutant factors confer hyperre
200 tivation was induced by treating CaMKII with diamide or histamine chloramine, two thiol-oxidizing age
201 the treatment of footprinting reactions with diamide or hydrogen peroxide.
202 f cellular proteins by incubating cells with diamide or incubating cellular extracts with GSSG oxidiz
203   In cells treated with the oxidizing agents diamide or phenylarsine oxide, S6K1 phosphorylation incr
204 utyl hydroperoxide, cumene hydroperoxide, or diamide) or by addition of Zn2+.
205 creased after exposure of M. tuberculosis to diamide; out of these, 39 were not induced in the sigH m
206                                        Using diamide oxidation and chemical cross-linking of the prot
207 inhibited after incubation with the oxidants diamide, oxidized glutathione, or hydrogen peroxide or w
208 64 microM), and the crystal structure of the diamide-oxidized protein was determined to be nearly ide
209  genes, although transcription is induced by diamide, Oxs1 or Pap1 plays a negative role with full de
210 opentadienylmono(oxazolinyl)borato zirconium diamide {Ph2B(C5H4)(Ox(4S-iPr,Me2))}Zr(NMe2)2.
211                        Low concentrations of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU)
212 esence exaggerated the suppressive effect of diamide plus BCNU.
213                                              Diamide plus BSO-induced thiol/disulfide imbalance was a
214          Here we show that a simple tertiary diamide precipitates gold selectively from aqueous acidi
215                                              Diamide pretreatment increased the sensitivity of HAECs
216                          Optimization of the diamide prodrugs of phosphonic acid 2a (MB05032) led to
217 ells, an exposure to the oxidant H(2)O(2) or diamide produced concentration-dependent inhibitions of
218     The time course for the synthesis of the diamide product and positional isotope exchange experime
219  and the synthesis of the cobyrinic acid a,c-diamide product are uncoupled.
220 gma(H) induction, we exposed both strains to diamide, rapidly washed it away, and resumed culturing i
221 servation that the disruption of spectrin by diamide reduces force generation in the cell.
222  residues does not similarly affect H2O2 and diamide regulation of yAP-1 function.
223     These desirable properties of phosphonic diamides represent significant improvements over existin
224 -CRD), that is required for H(2)O(2) but not diamide resistance and influences the localization of th
225 er the up-regulation of PxRyR is involved in diamide resistance remains unknown.
226 nce but does not contribute significantly to diamide resistance.
227 olerance from promoters of genes involved in diamide resistance.
228 ver from oxidant insults of 20 and 40 microM diamide, respectively.
229 the sulfydryl-oxidizing agents, H(2)O(2) and diamide, result in diminished RyR2-FKBP12.6 binding.
230                      Treatment of cells with diamide resulted in a dose-dependent increase in the GSS
231 atment of the affinity-purified enzymes with diamide resulted in the formation of disulfide bonds and
232          Treatment of intact PC12 cells with diamide results in a concentration-dependent inhibition
233 P-2 inhibitors introduced a cyclic tartronic diamide scaffold.
234 with aryl chlorides and bromides, two oxalic diamides serve as the powerful ligands.
235          Mouse fibroblast cells treated with diamide showed a reversible decrease in cAPK activity.
236  with either adriamycin or the thiol oxidant diamide showed elevated levels of glutathione disulfide
237 ne dicarboxylic acid bis[N,N-dimethylamide] (diamide), significantly reduced this interaction.
238 ral reorganisation of the initially chelated diamide spectator ligand, computational quantum chemical
239               Here we show that two pyridine diamide-strapped calix[4]pyrroles induce coupled chlorid
240 sumed culturing in diamide-free medium (post-diamide stress culturing).
241 a(H) (Delta-sigma(H)) is more susceptible to diamide stress than wild-type M. tuberculosis.
242 ranscriptional reprogramming-the response to diamide stress.
243 ng to the sigH regulon, especially following diamide stress.
244                     Fluorescent alpha,alpha'-diamide substituted bi- and terthiophene derivatives wer
245 mol for unsubstituted DBCOD to 68 kJ/mol for diamide-substituted DBCOD.
246 tramolecular hydrogen bonding formed by 1,10-diamide substitution stabilizes Boat, spiking the temper
247                                              Diamides, such as flubendiamide and chlorantraniliprole,
248 ferent ox-HSF1 conformers in the presence of diamide, suggesting that C3 could be disulfide cross-lin
249      The sulfhydryl-reactive oxidative agent diamide suppressed LTC(4)S activity and induced a revers
250 4,6-dioxopirimidines are designed as key 1,3-diamide surrogates that perform exceedingly in amine-squ
251                           Cobyrinic acid a,c-diamide synthetase from Salmonella typhimurium (CbiA) is
252                  Monoesters, monoamides, and diamides tested generally exhibited low in vitro activit
253 H(2)O(2) and more sensitive to menadione and diamide than wild-type cells.
254 lity (22-47%) was achieved using phosphonate diamides that convert to the corresponding phosphonic ac
255  [gamma-18O4]-ATP and adenosyl cobyrinic a,c-diamide the enzyme will catalyze the positional isotope
256 ug menadione, the sulfhydryl-oxidizing agent diamide, the disulfide-reducing agent dithiothreitol, hy
257 ing pretreatment of mitochondria with TBH or diamide, the Ki for ADP increased to 50-100 microM, wher
258 on is enhanced by exposure to either H2O2 or diamide, the protein responds to the oxidative stress pr
259 ocrystal featuring biaxial coordination of a diamide to the unhindered iodolium compound.
260 The addition of increasing concentrations of diamide to these cells resulted in oxidation of the acti
261 otonate the NH center in the five-coordinate diamides to give the amido-amine, e.g., [Cp*Ir(TsDPEN)](
262 d upon the addition of a recognized oxidant (diamide) to the RBC sample followed by a subsequent retu
263 n the use of pharmacological agents, such as diamide, to alter the UCP3 glutathionylation state.
264 uric acids, a subtype of pseudosymmetric 1,3-diamides, to yield the corresponding 5,5-disubstituted (
265 eractive in terms of their ability to confer diamide tolerance to cells but fail to provide even norm
266 rom 0.02 in untreated cells to > or = 0.5 in diamide-treated cells were accompanied by dose-dependent
267 ross-linked oxidized hHSF1 (ox-hHSF1) in the diamide-treated sample.
268                                              Diamide treatment caused partial release of Zn from ClpX
269 ntly induced at least 50-fold in response to diamide treatment in a sigR-dependent manner.
270 srA tag recognized by ClpXP was inhibited by diamide treatment in vitro.
271   Thus, we demonstrated that reperfusion and diamide treatment increased S-thiolation of a number of
272  medium during the recovery period following diamide treatment increased the extent of restoration of
273              This effect was also induced by diamide treatment of Ku and could be abrogated by dithio
274                                              Diamide treatment of NIH3T3 cells likewise induced poten
275                                        Thus, diamide treatment of nuclear extracts strongly reduces t
276 5)S]cysteine, to label cellular GSH prior to diamide treatment, followed by immunoprecipitation of TH
277 minates the methionine auxotrophy imposed by diamide treatment, suggesting that modulation of MetE ac
278 ve stress as induced by H2O2, menadione, and diamide treatment.
279 cA/ClpCP-catalyzed proteolysis in vitro, but diamide used at the concentrations that inhibited ClpXP
280 h various substrates, including diesters and diamides, via (1)H NMR spectroscopy and isothermal titra
281 ied after FKBP binding had occurred, whereas diamide was always effective.
282                                The effect of diamide was blocked by pretreatment with N-ethylmaleimid
283 n binding receptor based on dipicolinic acid diamide was equipped with thiol groups in the amidic sid
284                                      The 1,4-diamide was more potent across the tumor panel than the
285                                The effect of diamide was reversed by the addition of excess DTT, sugg
286                           The sensitivity to diamide was suppressed by deletion of the TRX2 gene.
287          We report that the efficacy of both diamides was dramatically reduced in clonal Sf9 cells st
288                                              Diamide weakly inactivated purified recombinant cPKC-alp
289 d when molar ratios of gammaC-crystallin-GSH-diamide were 1:2:5 and 1:10:25, respectively.
290                             These effects of diamide were dose-dependent and were rapidly and quantit
291 led to a greater extent only by paraquat and diamide, whereas they are less susceptible to the effect
292                                We found that diamide, which affects spectrin, reduces the axial stiff
293  sensitivity to oxidative stress agents like diamide, which are known to alter the oxidation reductio
294                                 Oxidation by diamide, which converts thiols to the disulfide, inactiv
295 of kinase activity to the sulfhydryl oxidant diamide, which inhibited by promoting an intramolecular
296     They are only slightly hypersensitive to diamide, which is nitrogen source-dependent, and minimal
297 cid halides furnished the corresponding N,N'-diamides, which were converted into N,N'-dithioamides by
298 the resulting CCl3 ketone to form a range of diamides with high diastereo- and enantioselectivity (up
299 including tert-butyl hydroperoxide (tBH) and diamide without affecting cell proliferation, baseline a
300 ith the newly prepared zinc-deuteroporphyrin diamide (ZnMb(diamide), 3), which converts the charged g

 
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