ライフサイエンスコーパス: diamide

1 , and the calcium-activated calcium channel (diamides).

2 as examined using the thiol-specific oxidant diamide.

3 crosslinking of transmembrane cysteines with diamide.

4 e, and g within adenosyl cobyrinic acid a,c-diamide.

5 ells treated with the thiol-specific oxidant diamide.

6 hydrogen peroxide, menadione, paraquat, and diamide.

7 ene hydroperoxide, t-butyl hydroperoxide, or diamide.

8 lted in the production of cobyrinic acid a,c-diamide.

9 tolerance but dispensable for resistance to diamide.

10 by amidation to form Ni-sirohydrochlorin a,c-diamide.

11 tein is treated with strong oxidants such as diamide.

12 cued by the addition of the chemical oxidant diamide.

13 e to both H2O2 and the thiol-oxidizing agent diamide.

14 shock and the thiol-specific oxidizing agent diamide.

15 the formation of ox-hHSF1 in the presence of diamide.

16 y induced (70-fold) following treatment with diamide.

17 anothione disulfide following oxidation with diamide.

18 owth inhibition by the thiol-oxidizing agent diamide.

19 e inactivation of NFI by the oxidizing agent diamide.

20 ility to induce this activity on exposure to diamide.

21 formation of the intersubunit cross-links by diamide.

22 identical to that obtained in the absence of diamide.

23 the channel by the disulfide inducing agent, diamide.

24 s increased sensitivity to the thiol oxidant diamide.

25 rmeant bis-quaternary ammonium derivative of diamide.

26 C56S mutation was resistant to the effect of diamide.

27 nstrate increased resistance to both tBH and diamide.

28 amide, and expression of trxD was induced by diamide.

29 A1 increased cellular sensitivity to tBH and diamide.

30 FP-tagged TNFRs exposed to the thiol oxidant diamide.

31 tance to catechol, MHQ, 1,4-benzoquinone and diamide.

32 ate two important properties of these simple diamides.

33 In contrast, diamide 1) activates the channel, 2) enhances [3H]ryanod

34 tive double Heck cyclizations of cyclohexene diamides 1 and 3 form contiguous quaternary stereocenter

35 Treatment with high concentrations of diamide (1 mm) resulted in an increase in the FRET signa

36 reatment of cells with low concentrations of diamide (1 mum) that was not sufficient to provoke TNFR

37 for example, N,N,N'N'-tetrahexylpropane-1,3-diamide (1), N,N'-dibutyl-N,N'-dimethyl-2-tetradecylprop

38 nd eliminated the necessity of preparing the diamide 13.

39 ibutyl-N,N'-dimethyl-2-tetradecylpropane-1,3-diamide (2), or N,N,N'N'-tetramethylpropane-1,3-diamide

40 In situ imidazolate-4,5-diamide-2-olate linker generation leads to the formation

41 prepared zinc-deuteroporphyrin diamide (ZnMb(diamide), 3), which converts the charged groups to neutr

42 10 mm) and inhibited by the oxidizing agent diamide (30 mum).

43 abeled zinc porphyrin derivative (ZnMb((15)N-diamide), 4).

44 sporter mutants, Deltaatr1 and Deltaflr1, to diamide, 4-NQO, and cadmium.

45 sic internal aromatic amine of 3 to give the diamide 5.

46 mide (2), or N,N,N'N'-tetramethylpropane-1,3-diamide (6), are poorly organized for metal ion complexa

47 Diamide 7 was prepared, and the X-ray crystal structure

48 id 2a (MB05032) led to the identification of diamide 8 (MB06322), the first reported orally efficacio

49 peroxide, whereas they are more sensitive to diamide, a disulfide bond-inducing agent.

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

51 Control studies involving diamide, a membrane-stiffening agent, suggest that the R

52 of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces b

53 We showed that diamide, a reagent that promotes disulfide bond formatio

54 M containing 25 mM glucose were treated with diamide, a thiol oxidant, at a concentration that did no

55 ramide, whereas treatment of astrocytes with diamide, a thiol-depleting agent, alone caused degradati

56 Treatment with diamide, a thiol-oxidizing agent, induced formation of d

57 These diamides act on the ryanodine receptor (RyR), a large en

58 and cell lysates containing Sav mutants with diamide affords up to >100 TON's and only a modest erosi

59 cells treated with diethyl maleate (DEM) or diamide, agents that deplete cellular thiols, had increa

60 ibited by pro-oxidants hydrogen peroxide and diamide, although these two pro-oxidants by themselves h

61 Neutral N3S diamide amine thiol chelators with no adjacent positive

62 perimental and DFT study of the reactions of diamide-amine supported titanium hydrazides with alkynes

63 e inducible by exposure of cells to H2O2 and diamide, among other oxidative stress eliciting compound

64 vity to dithiothreitol, a reductant, whereas diamide, an oxidant had no effect on the growth of the m

65 data are consistent with a model in which 1) diamide, an oxidizing agent, simultaneously produces an

66 hylmaleimide (NEM), an alkylating agent, and diamide, an oxidizing agent, were examined for effects o

67 UVEC) monolayers for 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decrea

68 age at the alpha-carbon position through the diamide and alpha-amidation pathways.

69 Thiol reactive agents such as diamide and cadmium induce zinc efflux by interfering wi

70 Diamide and dithiothreitol were reagents used respective

71 tion 199 was resistant to inhibition by both diamide and glutathionylation, thus implicating this as

72 Although both diamide and H(2)O(2) have been used to impose oxidative

73 e stress elicited by the redox-active agents diamide and H(2)O(2).

74 ional residues upon exposure to pro-oxidants diamide and H2O2 Here we hypothesize that routine storag

75 d function by the action of oxidants such as diamide and hydrogen peroxide; however, prior DNA bindin

76 or the glutathione-specific oxidizing agent diamide and in whole newborn mouse eyes incubated in the

77 In contrast, the oxidizing agents diamide and menadione inhibited the development of hillo

78 Diamide and N-ethylmaleimide likewise inhibit the disloc

79 potential and/or free thiol status, such as diamide and N-ethylmaleimide.

80 erential sensitivity of their RNA binding to diamide and N-ethylmaleimide.

81 mutant was more sensitive to the effects of diamide and oxygen than the parent strain.

82 fluorescence and comparison to the oxidants diamide and phenylhydrazine revealed that oxidation does

83 vely) to serine rendered HSF1 insensitive to diamide and prevented its conversion to ox-HSF1.

84 Treatment of PTP1B with diamide and reduced glutathione or with only glutathione

85 In the presence of a low concentration of diamide and reduced glutathione, the kinase was rapidly

86 rsine oxide (PheArs) is greater than that by diamide and t-butylhydroperoxide (TBH), yet the increase

87 was also induced by the GSH-oxidizing agent diamide and the GSH-conjugating agent N-ethylmaleimide,

88 ed sensitivity to the thiol-specific oxidant diamide and to the redox cycling compounds menadione and

89 es of extractants (organophosphorus ligands, diamides and N-heterocycles), with a focus on the separa

90 elial cells with the thiol-specific oxidant, diamide, and assessed activities of the UPP.

91 The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to det

92 tective during exposure to the thiol oxidant diamide, and expression of trxD was induced by diamide.

93 esulted in increased sensitivity to benomyl, diamide, and menadione, but not 4-NQO, cycloheximide, or

94 tment of mouse brain synaptosomes with H2O2, diamide, and sodium nitroprusside caused aggregation of

95 also produced 1-desmethylcobyrinic acid a,c-diamide, and strains that had neither cbiP nor cbiA synt

96 the present study, we examined the effect of diamide, and the model oxidant hydrogen peroxide (H(2)O(

97 partially inhibited by N-ethylmaleimide and diamide, and unaffected by arsenite.

98 Diamide appears to oxidize particular cysteine residues

99 In addition, single channels activated by diamide are further activated by the addition of NEM.

100 ortho- and para-benzoquinones which act like diamide as thiol-reactive electrophiles.

101 in vivo is reduced when cells are exposed to diamide, as shown by the enhanced stability of an SsrA-t

102 ious concentrations of glutathione (GSH) and diamide at 25 degrees C for 1 hour.

103 Diamide at concentrations of up to 5 mM reduced the axia

104 iolation, we used the thiol-specific oxidant diamide because its oxidant activity is restricted to in

105 the double mutant R91C/G98D was resistant to diamide block.

106 ar proteins also shows that sulforaphane and diamide, both known to react with cysteine amino acids,

107 ese mutant factors confer hyperresistance to diamide but hypersensitivity to H(2)O(2).

108 bsence of ATP or adenosyl cobyrinic acid a,c-diamide, but the rate of glutamine hydrolysis is enhance

109 Moreover, the oxidant diamide can restore growth and secretion in ero1 mutants

110 to thiol-specific stress conditions, such as diamide, catechol and 2-methylhydroquinone (MHQ).

111 Diamide caused a rapid increase in oxidized glutathione

112 cordings and inside-out patches, H(2)O(2) or diamide caused a strong inhibition of the vascular K(ATP

113 Oxidation of GSH with the thiol oxidant diamide caused significant decreases in cellular GSH and

114 ning approach and identified a benzimidazole diamide compound designated GSK669 that selectively inhi

115 Oxidizing agents, in particular diamide, could further enhance transcription of the trxB

116 When incubated with oxygen or diamide, CprK undergoes inactivation; subsequent treatme

117 The corresponding diamide derivative was also synthesized and analyzed fro

118 These results imply that the diester or diamide derivatives of the d-tetrapeptides self-assemble

119 Phosphonic diamides derived from amino acid esters were discovered

120 ation of a novel benzylpiperazine adamantane diamide-derived compound that inhibits EboV infection.

121 Notably, H(2)O(2) and diamide differentially affected the RyR2-FKBP12.6 intera

122 A diamide diimine ligand, [{-CH=N(1,2-C6H4)NH(2,6-iPr2C6H3

123 Moreover, in both HAECs and BAECs, diamide dramatically increased both the rate and magnitu

124 When examined for promoters up-regulated by diamide, effective Pap1 binding to these targets require

125 All diamide effects can be reversed by the reducing agent, d

126 Diamide either cross-links phase 1 sulfhydryls or causes

127 l modification by N-ethylmaleimide (NEM) and diamide, even under conditions that led to severe cellul

128 atment with the sulfhydryl oxidizing reagent diamide formed the faster migrating, slower dissociating

129 dly washed it away, and resumed culturing in diamide-free medium (post-diamide stress culturing).

130 TP-dependent synthesis of cobyrinic acid a,c-diamide from cobyrinic acid using either glutamine or am

131 nsformations to afford a wide variety of 1,2-diamide functionalized products.

132 phosphotyrosine residue, and a diester or a diamide group, we find that, regardless of the stereoche

133 Loss of TH catalytic activity caused by diamide-GSH is partially recovered by DTT and glutaredox

134 The effect of diamide-GSH on TH activity is prevented by dithiothreito

135 were inhibited strongly by a combination of diamide/GSH or H(2)O(2)/GSH but not by either alone.

136 e in binding strength between the urea and a diamide guest in 0.1 M NBu4B(C6F5)4/CH2Cl2.

137 Similar to diamide, H(2)O(2) increased the sensitivity of HAECs to

138 Diamide had no effect on the C150S mutant enzyme, sugges

139 s and treated with three oxidative reagents (diamide, hydrogen peroxide, and phenylhydrazine) to cros

140 ns but can be oxidized by the strong oxidant diamide, implying that the redox potential for the thiol

141 mine, is inhibited by the sulfhydryl oxidant diamide in a concentration-dependent manner.

142 loss of sensitivity to both sulforaphane and diamide in electrophoretic mobility shift assay analysis

143 Treatment of TH with diamide in the presence of [(35)S]GSH results in the inc

144 ance to two different oxidants, H(2)O(2) and diamide, in cells that contain an intact glutamate catab

145 Likewise, GSH markedly potentiated diamide inactivation of a PKC isozyme mixture purified f

146 Diamide inactivation of cPKC-alpha and its potentiation

147 the heme diester or, for the first time, the diamide increases the second-order rate constant of the

148 train produced 1-desmethylcobyrinic acid a,c-diamide, indicating that CbiD is involved in C-1 methyla

149 cetyl cysteine attenuated GSSG elevation and diamide-induced apoptosis.

150 Diamide-induced blocking was reversed by disulfide bond-

151 GSH potentiation of diamide-induced cPKC-alpha inactivation was associated w

152 We describe a Pap1-Oxs1 pathway for diamide-induced disulfide stress in Schizosaccharomyces

153 Diamide-induced expression of trxC, trxE, and trxF incre

154 Diamide-induced formation of the Cys-150 disulfide bond

155 Diamide induces intersubunit dimer formation of both the

156 reincubation of the latent HSF1 monomer with diamide inhibited the in vitro heat-induced activation a

157 thermore, oxidizing agents, such as H2O2 and diamide, inhibited Gag processing of wild-type virions,

158 vidence that the G4946E RyR mutation impairs diamide insecticide binding.

159 dine receptor (RyR) was highly correlated to diamide insecticide resistance in field populations of P

160 cation enzymes have been associated with the diamide insecticide resistance in the diamondback moth,

161 Recently acquired resistance to diamide insecticides in this species is thought to be du

162 The recent introduction of synthetic diamide insecticides, with a novel mode of action, poten

163 Calcium pulstrodes based on the diamide ionophore AU-1 were characterized and applied to

164 Diamide is a chemical oxidant that selectively converts

165 to treatment with the thiol-specific oxidant diamide is the result of transcription initiation at the

166 r conditions in which cAPK is inactivated by diamide, it is also readily thiolated.

167 III alkyl complexes supported by a ferrocene diamide ligand (1,1'-fc(NSi(t)BuMe(2))(2)) have been fou

168 -sandwich complexes supported by a ferrocene diamide ligand (NN(fc)) are reported.

169 Utilizing a rigid ferrocene diamide ligand (NN(TBS)), a Dy(III) SIM, (NN(TBS))DyI(TH

170 a) benzyl complexes supported by a ferrocene diamide ligand are reactive toward aromatic N-heterocycl

171 yridyl complex supported by a 1,1'-ferrocene diamide ligand is reported.

172 nzyl complexes supported by a ferrocene 1,1'-diamide ligand.

173 benzyl complex supported by a ferrocene 1,1'-diamide ligand.

174 t, thus demonstrating the potential of rigid diamide ligands in the design of new SIMs with defined m

175 Inhibition of TNF-alpha- and diamide-mediated depletion of GSH, elevation of ceramide

176 of Deltayap1 cells to the oxidants H(2)O(2), diamide, menadione and tert-butyl hydroperoxide.

177 rial libraries of dimeric iminodiacetic acid diamides, novel small molecule binders of EPOr were iden

178 Mitochondrial dysfunction in response to diamide occurred in stages, progressing from oscillation

179 um(0) and the chiral ligand derived from the diamide of trans-1,2-diaminocyclohexane and 2-diphenylph

180 sm, we report the semisynthesis of mono- and diamides of biliverdin IXalpha and those of its non-natu

181 were rapidly linked through oxidation (with diamide) of the Cys 73 disulfide bond, and the relative

182 The inhibitory effect of diamide on TH catalytic activity is enhanced significant

183 ap1 form a complex when cells are exposed to diamide or Cd that causes disulfide stress.

184 cellular Ca(2+), acute treatment with either diamide or H(2)O(2) increased the number of BAECs exhibi

185 xB gene was induced following treatment with diamide or H(2)O(2) or exposure to oxygen.

186 he same high level in the presence of either diamide or H(2)O(2), these mutant factors confer hyperre

187 the treatment of footprinting reactions with diamide or hydrogen peroxide.

188 f cellular proteins by incubating cells with diamide or incubating cellular extracts with GSSG oxidiz

189 In cells treated with the oxidizing agents diamide or phenylarsine oxide, S6K1 phosphorylation incr

190 utyl hydroperoxide, cumene hydroperoxide, or diamide) or by addition of Zn2+.

191 creased after exposure of M. tuberculosis to diamide; out of these, 39 were not induced in the sigH m

192 Using diamide oxidation and chemical cross-linking of the prot

193 inhibited after incubation with the oxidants diamide, oxidized glutathione, or hydrogen peroxide or w

194 64 microM), and the crystal structure of the diamide-oxidized protein was determined to be nearly ide

195 genes, although transcription is induced by diamide, Oxs1 or Pap1 plays a negative role with full de

196 opentadienylmono(oxazolinyl)borato zirconium diamide {Ph2B(C5H4)(Ox(4S-iPr,Me2))}Zr(NMe2)2.

197 Low concentrations of diamide plus 1,3-bis(2 chloroethyl)-1-nitrosourea (BCNU)

198 esence exaggerated the suppressive effect of diamide plus BCNU.

199 Diamide plus BSO-induced thiol/disulfide imbalance was a

200 Diamide pretreatment increased the sensitivity of HAECs

201 Optimization of the diamide prodrugs of phosphonic acid 2a (MB05032) led to

202 ells, an exposure to the oxidant H(2)O(2) or diamide produced concentration-dependent inhibitions of

203 The time course for the synthesis of the diamide product and positional isotope exchange experime

204 and the synthesis of the cobyrinic acid a,c-diamide product are uncoupled.

205 gma(H) induction, we exposed both strains to diamide, rapidly washed it away, and resumed culturing i

206 servation that the disruption of spectrin by diamide reduces force generation in the cell.

207 residues does not similarly affect H2O2 and diamide regulation of yAP-1 function.

208 These desirable properties of phosphonic diamides represent significant improvements over existin

209 -CRD), that is required for H(2)O(2) but not diamide resistance and influences the localization of th

210 er the up-regulation of PxRyR is involved in diamide resistance remains unknown.

211 nce but does not contribute significantly to diamide resistance.

212 olerance from promoters of genes involved in diamide resistance.

213 ver from oxidant insults of 20 and 40 microM diamide, respectively.

214 the sulfydryl-oxidizing agents, H(2)O(2) and diamide, result in diminished RyR2-FKBP12.6 binding.

215 Treatment of cells with diamide resulted in a dose-dependent increase in the GSS

216 atment of the affinity-purified enzymes with diamide resulted in the formation of disulfide bonds and

217 Treatment of intact PC12 cells with diamide results in a concentration-dependent inhibition

218 Mouse fibroblast cells treated with diamide showed a reversible decrease in cAPK activity.

219 with either adriamycin or the thiol oxidant diamide showed elevated levels of glutathione disulfide

220 ne dicarboxylic acid bis[N,N-dimethylamide] (diamide), significantly reduced this interaction.

221 Here we show that two pyridine diamide-strapped calix[4]pyrroles induce coupled chlorid

222 sumed culturing in diamide-free medium (post-diamide stress culturing).

223 a(H) (Delta-sigma(H)) is more susceptible to diamide stress than wild-type M. tuberculosis.

224 ranscriptional reprogramming-the response to diamide stress.

225 ng to the sigH regulon, especially following diamide stress.

226 Fluorescent alpha,alpha'-diamide substituted bi- and terthiophene derivatives wer

227 Diamides, such as flubendiamide and chlorantraniliprole,

228 ferent ox-HSF1 conformers in the presence of diamide, suggesting that C3 could be disulfide cross-lin

229 The sulfhydryl-reactive oxidative agent diamide suppressed LTC(4)S activity and induced a revers

230 4,6-dioxopirimidines are designed as key 1,3-diamide surrogates that perform exceedingly in amine-squ

231 Cobyrinic acid a,c-diamide synthetase from Salmonella typhimurium (CbiA) is

232 Monoesters, monoamides, and diamides tested generally exhibited low in vitro activit

233 H(2)O(2) and more sensitive to menadione and diamide than wild-type cells.

234 lity (22-47%) was achieved using phosphonate diamides that convert to the corresponding phosphonic ac

235 [gamma-18O4]-ATP and adenosyl cobyrinic a,c-diamide the enzyme will catalyze the positional isotope

236 ug menadione, the sulfhydryl-oxidizing agent diamide, the disulfide-reducing agent dithiothreitol, hy

237 ing pretreatment of mitochondria with TBH or diamide, the Ki for ADP increased to 50-100 microM, wher

238 on is enhanced by exposure to either H2O2 or diamide, the protein responds to the oxidative stress pr

239 The addition of increasing concentrations of diamide to these cells resulted in oxidation of the acti

240 otonate the NH center in the five-coordinate diamides to give the amido-amine, e.g., [Cp*Ir(TsDPEN)](

241 d upon the addition of a recognized oxidant (diamide) to the RBC sample followed by a subsequent retu

242 n the use of pharmacological agents, such as diamide, to alter the UCP3 glutathionylation state.

243 uric acids, a subtype of pseudosymmetric 1,3-diamides, to yield the corresponding 5,5-disubstituted (

244 eractive in terms of their ability to confer diamide tolerance to cells but fail to provide even norm

245 rom 0.02 in untreated cells to > or = 0.5 in diamide-treated cells were accompanied by dose-dependent

246 ross-linked oxidized hHSF1 (ox-hHSF1) in the diamide-treated sample.

247 Diamide treatment caused partial release of Zn from ClpX

248 ntly induced at least 50-fold in response to diamide treatment in a sigR-dependent manner.

249 srA tag recognized by ClpXP was inhibited by diamide treatment in vitro.

250 Thus, we demonstrated that reperfusion and diamide treatment increased S-thiolation of a number of

251 medium during the recovery period following diamide treatment increased the extent of restoration of

252 This effect was also induced by diamide treatment of Ku and could be abrogated by dithio

253 Diamide treatment of NIH3T3 cells likewise induced poten

254 Thus, diamide treatment of nuclear extracts strongly reduces t

255 5)S]cysteine, to label cellular GSH prior to diamide treatment, followed by immunoprecipitation of TH

256 minates the methionine auxotrophy imposed by diamide treatment, suggesting that modulation of MetE ac

257 ve stress as induced by H2O2, menadione, and diamide treatment.

258 cA/ClpCP-catalyzed proteolysis in vitro, but diamide used at the concentrations that inhibited ClpXP

259 ied after FKBP binding had occurred, whereas diamide was always effective.

260 The effect of diamide was blocked by pretreatment with N-ethylmaleimid

261 n binding receptor based on dipicolinic acid diamide was equipped with thiol groups in the amidic sid

262 The 1,4-diamide was more potent across the tumor panel than the

263 The effect of diamide was reversed by the addition of excess DTT, sugg

264 The sensitivity to diamide was suppressed by deletion of the TRX2 gene.

265 We report that the efficacy of both diamides was dramatically reduced in clonal Sf9 cells st

266 Diamide weakly inactivated purified recombinant cPKC-alp

267 d when molar ratios of gammaC-crystallin-GSH-diamide were 1:2:5 and 1:10:25, respectively.

268 These effects of diamide were dose-dependent and were rapidly and quantit

269 led to a greater extent only by paraquat and diamide, whereas they are less susceptible to the effect

270 We found that diamide, which affects spectrin, reduces the axial stiff

271 sensitivity to oxidative stress agents like diamide, which are known to alter the oxidation reductio

272 Oxidation by diamide, which converts thiols to the disulfide, inactiv

273 of kinase activity to the sulfhydryl oxidant diamide, which inhibited by promoting an intramolecular

274 They are only slightly hypersensitive to diamide, which is nitrogen source-dependent, and minimal

275 the resulting CCl3 ketone to form a range of diamides with high diastereo- and enantioselectivity (up

276 including tert-butyl hydroperoxide (tBH) and diamide without affecting cell proliferation, baseline a

277 ith the newly prepared zinc-deuteroporphyrin diamide (ZnMb(diamide), 3), which converts the charged g