ライフサイエンスコーパス: NEM

1 NEM (100 microM) alone had no significant effect on rest

2 NEM (5 mm) decreased, increased, and then decreased the

3 NEM added during calyculin A stimulation, i.e. during th

4 NEM alone and in concert with PDGF-BB increased reactive

5 NEM also abrogated the phosphorylation of p70S6K, riboso

6 NEM also reduced with no lysine (WNK) kinase phosphoryla

7 NEM and diethyl pyrocarbonate inhibition suggested that

8 NEM decreased while TPA increased TRH levels in rat hypo

9 NEM increased the P(o) of KCNQ2, KCNQ4, and KCNQ5 by thr

10 NEM induced a dose-dependent increase in the readily rel

11 NEM inoculation specifically promoted mural cell coverag

12 NEM irreversibly activated M159C TASK-3, with minimal ef

13 NEM labeling at 0 degrees C indicates that alkylation of

14 NEM modification altered nucleotide-dependent changes in

15 NEM modification had no effect on the basal ATPase rate

16 NEM modification increased the ANS fluorescence of Ssa1p

17 NEM treatment of HIV-1 or SIV resulted in extensive cova

18 NEM-modified M159C channels were resistant to inhibition

19 NEM-S1 dramatically reduced both the extent and rate of

20 NEM-S1, a strong-binding non-tension-generating derivati

21 NEM-sensitive factor (NSF) is an essential protein requi

22 thylmaleimide-modified myosin subfragment 1 (NEM-S1) at both short and long SLs.

23 ethylmaleimide-treated myosin subfragment 1 (NEM-S1) to actin filaments mimics such strong interactio

24 binding derivative of myosin subfragment 1 (NEM-S1).

25 nerating derivative of myosin subfragment-1 (NEM-S1) in chemically skinned myocardium from adult rats

26 and N-ethyl-maleimide myosin subfragment-1 (NEM-S1), a non-tension-generating, strong binding deriva

27 ylmaleimide-conjugated myosin subfragment-1 (NEM-S1), a strongly binding myosin analogue that coopera

28 e-generating analog of myosin subfragment-1 (NEM-S1).

29 reagent N-[ethyl-1-14C]ethylmaleimide ([14C]NEM) is used to detect site-directed alkylation of engin

30 idues is also determined by blockage of [14C]NEM labeling with membrane-impermeant thiol reagents suc

31 Interestingly, in the absence of Ca(2+) NEM-S1-induced activation of S1 ATPase was significantly

32 At fixed [Ca(2+)], NEM-S1 reduced the curvature of length traces and sped l

33 Labeling of MC1 with [3H]NEM indicated that enhanced MT binding was associated wi

34 ual zinc finger domain as a function of d(5)-NEM pulse time.

35 kylating reagent d(5)-N-ethylmaleimide (d(5)-NEM) is used as a residue-specific probe of the relative

36 ion of d(5),d(5)-, d(5),H(5)-, and H(5),H(5)-NEM derivatized peptides corresponding to each individua

37 hase with excess H(5)-N-ethylmaleimide (H(5)-NEM) to fully derivatize MTF-zf concomitant with complet

38 leimide (WPI+NEM) or 20mM added NaCl and 5mM NEM (WPI+NaCl+NEM).

39 A NEM composed of ChNP with CIzyme high intact C1 collagen

40 to Hb A, especially rHb (betaC93L) and Hb A-NEM in the NO form.

41 chemically modified Hb As, Hb A-IAA and Hb A-NEM, in which the sulfhydryl group at beta93Cys is modif

42 In addition, NEM blocked PDGF-BB-induced phosphorylation of BAD and f

43 In addition, NEM modification of subunit c was dependent upon the pre

44 onential- and stationary-phase cells against NEM.

45 involved in protecting E. coli cells against NEM.

46 ate affords no protection whatsoever against NEM inactivation of transport or alkylation with [(14)C]

47 with the membrane-permeant alkylating agent NEM.

48 Although NEM seems to be significantly more reliable based on the

49 reticulum membrane (microsomal GPAT) and an NEM-resistant form in the outer mitochondrial membrane (

50 reassembly stacking protein 65 (GRASP65), an NEM-sensitive membrane-bound component, is required for

51 ed calcium spikes in Mb axon terminals in an NEM-sensitive manner, but light responses above cone thr

52 New Ag+- and NEM-sensitive residues were found at the cytoplasmic end

53 ential maximal P(o), channel expression, and NEM action between the two channels.

54 transport activity, membrane expression, and NEM sensitivity are documented.

55 augmentation of KCNQ2, KCNQ4, and KCNQ5, and NEM pretreatment reduced Ca2+/CaM-mediated suppression o

56 The oxidized and NEM alkylated forms of human RNase H1 exhibited binding

57 ined by digesting the reduced, oxidized, and NEM-treated forms of human RNase H1 with trypsin and ana

58 ient serum (or even less) to measure PSA and NEM even in a non-cancer individual.

59 's conformation, the structures of Ssa1p and NEM-modified Ssa1p (NEM-Ssa1p) were compared using a var

60 nces in the secondary structure of Ssa1p and NEM-Ssa1p, and in their complexes with nucleotides.

61 Included among the maleimide reagents are NEM (n-ethylmaleimide) and several poly(ethylene glycol)

62 chip that can reliably detect PSA as well as NEM in patient samples has been developed.

63 d from a limited cohort, currently available NEM ELISA is not suitable for undertaking a large study.

64 pe hBAT with the substrate cholyl-CoA before NEM treatment prevented loss of N-acyltransferase activi

65 In bilayers, NEM (0.2 mm) increased P(o) of RyRs within seconds when

66 nterestingly, pretreatment with MTSES blocks NEM labeling of all the mutants.

67 NPG blocks NEM alkylation of Cys148 with an apparent affinity of ap

68 pha(q) protein were more-slowly activated by NEM, which suggests protection of Cys-159, and similar r

69 e49, Gln60, Ser67, or Leu70 are alkylated by NEM at 25 degrees C in 10 min, and mutants with Cys in p

70 of the transmembrane domain are alkylated by NEM at 25 degrees C, a mutant with Cys at position 315 a

71 most Cys replacements are also alkylated by NEM except for positions that face the bilayer.

72 on alone ablated most of the augmentation by NEM, suggesting that NEM acts via alkylation of this res

73 ulin A alone or with calyculin A followed by NEM were no longer sensitive to volume, isoproteronol or

74 The augmentation of submaximal force by NEM-S1 was accompanied by a marked reduction in the stee

75 en Ser mutants are completely inactivated by NEM, while Cys122-->Ser permease is insensitive to the s

76 mitoyl-CoA, was sensitive to inactivation by NEM, was inhibited by dihydroxyacetone phosphate and pol

77 NAC also attenuated the apoptosis induced by NEM, alone or in combination with PDGF-BB.

78 teine-less mutant was no longer inhibited by NEM, suggesting that inhibition occurs through modificat

79 ut neither y(+)LAT isoform, are inhibited by NEM.

80 uence channel opening and that inhibition by NEM modification was in part due to decreased ATP bindin

81 of incubation (0.5-5 min), and inhibition by NEM was partially reversed at short (0.5 min) and longer

82 cysteine 3635 of RYR1 is rapidly labeled by NEM and that this labeling is blocked by bound calmoduli

83 between residue 766 and 804 were modified by NEM and PEG-mal only in the presence of SDS, consistent

84 etween residues 744 and 761 were modified by NEM but not PEG-mal in the absence of SDS, suggesting a

85 on of PDGF-BB-induced Akt phosphorylation by NEM was completely reversed by PP2A inhibitors fostrieci

86 e disruption of NC zinc finger structures by NEM blocks early postentry steps in the retroviral infec

87 of all double Cys-to-Ala mutants with [(14)C]NEM demonstrated that seHAS contains no disulfide bonds.

88 [(14)C]NEM labeling of 13 single-Cys mutants, including the nin

89 [(14)C]NEM modification of C99A/C450A revealed one additional r

90 ation of transport or alkylation with [(14)C]NEM.

91 Thus, at low concentrations, NEM does not act as a selective thiol reagent and activa

92 Consequently, NEM-S1 eliminated any Ca(2+) dependence of relative powe

93 with samples homogenized in MeOH containing NEM.

94 used mouse brains with a solution containing NEM which reacts with the sulfhydryl group of GSH, thus

95 Nonspecific protease treatment of MNP-d9/.NEM-CcO converted its spectrum from that of an immobiliz

96 only residues modified by biotin-derivatized NEM in clorgyline-inactivated MAO A and pargyline-inacti

97 dues are also modified by biotin-derivatized NEM in the mitochondrial membrane-bound MAO A and MAO B.

98 adjoining loops, with N-[14C]ethylmaleimide (NEM) or methanethiosulfonate ethylsulfonate (MTSES) was

99 l-specific reagents N-[(14)C]ethylmaleimide (NEM) and methanethiosulfonate ethylsulfonate (MTSES) whi

100 cement mutants with N-[(14)C]ethylmaleimide (NEM) in right-side-out membrane vesicles.

101 cement mutants with N-[(14)C]ethylmaleimide (NEM) in the absence or presence of ligand.

102 ed by site-directed N-[(14)C]ethylmaleimide (NEM) labeling of the substrate-protectable Cys148 in the

103 sted are labeled by N-[(14)C]ethylmaleimide (NEM).

104 ious studies proposed that N-ethylmaleimide (NEM) alkylates 3 classes of thiols on skeletal muscle ry

105 lfhydryl-blocking reagents N-ethylmaleimide (NEM) and bis-dithionitrobenzoic acid (DTNB) prevented co

106 ysteine alkylating reagent N-ethylmaleimide (NEM) and by site-directed mutagenesis of the triad resid

107 ulfhydryl reagents such as N-ethylmaleimide (NEM) and iodoacetamide in a dose-dependent and time-depe

108 Sensitivity to N-ethylmaleimide (NEM) and methanethiosulfonate reagents was localized to

109 by the vesicle inhibitors N-ethylmaleimide (NEM) and monensin.

110 tes: Both were modified by N-ethylmaleimide (NEM) and Ser-substituted mutants retained partial activi

111 Chemical labeling with N-ethylmaleimide (NEM) and tandem mass spectrometry experiments clearly sh

112 membrane permeant reagent N-ethylmaleimide (NEM) and the membrane impermeant reagent polyethylenegly

113 -specific alkylating agent N-ethylmaleimide (NEM) as well as the reversible thiol-specific blockers p

114 Alkylation of RYR1 with N-ethylmaleimide (NEM) blocks both (35)S-apocalmodulin binding and oxidati

115 To determine if N-ethylmaleimide (NEM) can inactivate human immunodeficiency virus type 1

116 ted the mechanism by which N-ethylmaleimide (NEM) enhances transporter activity using a combination o

117 e cysteine-modifying agent N-ethylmaleimide (NEM) has been shown to inhibit system y(+) (most likely

118 to the toxic electrophile N-ethylmaleimide (NEM) have been investigated.

119 to the sulfhydryl reagent N-ethylmaleimide (NEM) in a manner similar to that of lac permease.

120 lfhydryl-modifying reagent N-ethylmaleimide (NEM) inactivates the yeast Hsp70 Ssa1p by reacting with

121 One millimolar N-ethylmaleimide (NEM) inhibited both MgATP-dependent and MgATP-independen

122 N-Ethylmaleimide (NEM) inhibited cotransport and also blocked the stimulat

123 cysteine-modifying reagent N-ethylmaleimide (NEM) is known to augment currents from native M-channels

124 thiol groups on the MPI by N-ethylmaleimide (NEM) markedly reduced this rate constant to kMPI-NEM=1.3

125 MAO A is inactivated by N-ethylmaleimide (NEM) much faster (tau(1/2) = approximately 3 min) than M

126 m temperature with 0.42 mM N-ethylmaleimide (NEM) or 0.42 mM iodoacetamide, respectively.

127 cell cytosol treated with N-ethylmaleimide (NEM) or phenyl-Sepharose to inactivate or deplete Crm1,

128 thiols on the enzyme with N-ethylmaleimide (NEM) prevented 5, 5-dimethyl-1-pyrroline N-oxide adduct

129 followed by treatment with N-ethylmaleimide (NEM) significantly inactivates the protein.

130 Oxidation as well as N-ethylmaleimide (NEM) treatment of human RNase H1 ablates the cleavage ac

131 N-ethylmaleimide (NEM) was used to mask free sulfhydryl groups present in

132 the reaction mechanism of N-ethylmaleimide (NEM) with free HIV-1 NCp7 protein.

133 he presence and absence of N-ethylmaleimide (NEM), a chemical that reacts irreversibly with free cyst

134 of Cys-159 modification by N-ethylmaleimide (NEM), a cysteine-selective alkylating agent.

135 Isomerase I inhibitor, and N-ethylmaleimide (NEM), a known LRAT inhibitor, significantly reduced Isom

136 N-Ethylmaleimide (NEM), a thiol alkylating agent, blocked PDGF-BB-induced

137 s possibility, we employed N-ethylmaleimide (NEM), an inhibitor of the ATPase N-ethylmaleimide-sensit

138 cells are pretreated with N-ethylmaleimide (NEM), an inhibitor of the endogenous aminophospholipid f

139 N-ethylmaleimide (NEM), and to a lesser extent, dithio(bis)-p-nitrobenzoat

140 and (616)GSSG), along with N-ethylmaleimide (NEM), and treated with acetonitrile to solubilize the en

141 reactive compounds such as N-ethylmaleimide (NEM), disulfiram, and organic disulfides [e.g., 2,2'-dit

142 reatment of the cells with N-ethylmaleimide (NEM), exogenous lipases such as sphingomyelinase and pho

143 nt but could be blocked by N-ethylmaleimide (NEM), indicating that NO acted via an S-nitrosylation me

144 pared the effectiveness of N-ethylmaleimide (NEM), iodoacetamide (IAM), and iodoacetic acid (IAA) in

145 s, iodoacetamide (IAA) and N-ethylmaleimide (NEM), respectively.

146 is completely inhibited by N-ethylmaleimide (NEM), suggesting that one or more of the seven native Cy

147 Pretreatment with N-ethylmaleimide (NEM), which occludes S-nitrosylation, or with 1-(2-trifl

148 N-Ethylmaleimide (NEM), which reacts readily with exposed sulfhydryl group

149 in TMH1 proved to be both N-ethylmaleimide (NEM)-sensitive and Ag+-sensitive and suggests a possible

150 oluble factors and soluble N-ethylmaleimide (NEM)-sensitive fusion protein (NSF) attachment protein r

151 d in mammalian tissues, an N-ethylmaleimide (NEM)-sensitive isoform in the endoplasmic reticulum memb

152 th that of the KCNQ opener N-ethylmaleimide (NEM).

153 12 cells were treated with N-ethylmaleimide (NEM).

154 lfhydryl alkylating agent, N-ethylmaleimide (NEM).

155 Cys291 of the enzyme with N-ethylmaleimide (NEM).

156 lfonate (MTS) reagents and N-ethylmaleimide (NEM).

157 e thiols are blocked using N-ethylmaleimide (NEM).

158 nt with the thiol reagent, N-ethylmaleimide (NEM).

159 ith a slight inhibition in N-ethylmaleimide (NEM, 1 mm)-treated RBCs and stimulation in RBCs untreate

160 isulfide is alkylated with N-ethylmaleimide (NEM-FTR).

161 nt, with the thiol-reactive N-ethylmalemide (NEM), results in modification of Cys327, suggesting that

162 switches in some applications--for example, NEM switches perform much better in extreme environments

163 However, the reverse transcriptase from NEM-treated virions remained active in exogenous templat

164 Furthermore, NEM-S1 potentiated submaximal Ca2+-activated forces and

165 Furthermore, NEM-S1 treatment reversibly eliminated the SL dependence

166 These differences give NEM switches an advantage over semiconductor switches in

167 with DAPI and antibodies directed against GS-NEM, glial fibrillary acidic protein (GFAP) in regions c

168 itu, prior to immunostaining with an anti-GS-NEM antibody.

169 r with analysis of the distribution of [(3)H]NEM labeling with each sequencing cycle, that cysteine 3

170 578C) was accessible to labeling with [(3)H]-NEM.

171 At high NEM-S1, the rates of wild-type and mutants approached th

172 P-insensitive, N-ethylmaleimide-treated HMM (NEM-HMM; 25-30%).

173 rations that did not activate RyRs inhibited NEM-induced Ca(2+) release, most likely by an interactio

174 markedly reduced this rate constant to kMPI-NEM=1.3 +/- 0.4 x 10(3)M(-1)s(-1) consistent with a key

175 M159W and M159F TASK-3 mutants behaved like NEM-modified M159C channels, with increased basal curren

176 We now show that low NEM concentrations (20-200 microm) elicit Ca(2+) release

177 lfhydryl alkylating agent N-ethyl maleimide (NEM) increased BK channel activity.

178 nvestigated the effect of N-ethyl-maleimide (NEM), an alkylating agent, and 12-O-tetradecanoylphorbol

179 covalent conjugation with N-ethyl-maleimide (NEM).

180 N-ethyl malemide (NEM), a sulfhydryl cross-linker, inhibited Nrf2 but not

181 protein, referred as neuroendocrine marker (NEM), is secreted only by malignant prostate cells and r

182 -free assay system that can reliably measure NEM and PSA in patient samples.

183 cysts either with Neff's encystment medium (NEM) or starvation on nonnutrient agar (NNA).

184 Treatment of skinned fibres with 5 microM NEM-S1 eliminated the low-velocity phase of shortening b

185 augmented threefold to fourfold by 50 microm NEM, and their voltage dependencies were negatively shif

186 control conditions, application of 6 microM NEM-S1 significantly increased Ca2+-independent tension,

187 Our results revealed that, within 15 min, NEM increased cell surface levels of KCC2 and modulated

188 We prepared a new enzyme mixture (NEM) composed of intact C1 and C2 collagenases and ChNP

189 edimentation assay, treatment with </=0.1 mM NEM enhanced MC1 binding to MTs in the presence of MgATP

190 In comparison, treatment with >/=0.5 mM NEM induced aggregation of MC1 and resulted in sedimenta

191 High (5 mm) NEM concentrations elicited SR Ca(2+) release that was n

192 (Nrp1) receptor (Nrp1-expressing monocytes; NEM).

193 of WT and cMyBP-C(-/-) myocardium with 3 muM NEM-S1 elicited similar increases in pCa(50,) but the ef

194 ons are the main cause of nemaline myopathy (NEM), with typical adult patients having low expression

195 oteins, than the heated WPI+NEM and WPI+NaCl+NEM solutions.

196 EM) or 20mM added NaCl and 5mM NEM (WPI+NaCl+NEM).

197 Nanoelectromechanical (NEM) switches are similar to conventional semiconductor

198 of 13 single-Cys mutants, including the nine NEM-sensitive Cys replacements, in right-side-out membra

199 kout of mtGPAT; however, we detected a novel NEM-sensitive GPAT activity in mitochondrial fractions a

200 acellular capsids isolated in the absence of NEM contain disulfide cross-linked species; however, int

201 uman RNase H1 in the presence and absence of NEM showed peptide masses consistent with the formation

202 In the absence of NEM-S1, maximal force and k(tr) and the pCa(50) of isome

203 In the absence of NEM-S1, the rate of force redevelopment (ktr) was found

204 s obtained at the same pCa in the absence of NEM-S1.

205 In particular, the addition of NEM-HMM increased a non-Gaussian tail in the path curvat

206 Addition of NEM-S1 reduced the Ca2+ dependence of ktr by eliciting m

207 of approximately 1.90 microm, application of NEM-S1 markedly increased submaximal Ca2+-activated tens

208 The Neb cKO phenocopies important aspects of NEM (muscle weakness, oxidative fiber-type predominance,

209 urating actin concentrations, the binding of NEM-modified S1 to actin-tropomyosin-troponin increases

210 The combination of NEM and synthetic PS scramblase enhances the ability of

211 ) was treated with varying concentrations of NEM (0-10 mM) and cosedimentation and ATPase assays were

212 In the presence of low concentrations of NEM-S1, wild-type troponin was more active than the muta

213 growing cells correlated with the degree of NEM sensitivity.

214 This effect of NEM was contingent upon prior treatment of the cells wit

215 The effect of NEM-S1 to increase low-velocity V(o) can be explained in

216 07 dephosphorylation mediated the effects of NEM on KCC2 activity.

217 lar increases in pCa(50,) but the effects of NEM-S1 to increase k(tr) at submaximal forces and thereb

218 l function, we investigated the mechanism of NEM action and subunit specificity of cloned KCNQ2-5 cha

219 Here we review the potential of NEM-switch technologies to complement or selectively rep

220 cellular capsids isolated in the presence of NEM are unstable; B and C capsids are converted to a nov

221 ved by denaturing the mAb in the presence of NEM in guanidine hydrochloride (GuHCl).

222 was 0.02+/-0.01 pCa units in the presence of NEM-S1 compared with a DeltapCa50 of 0.10+/-0.01 pCa uni

223 In the presence of NEM-S1, peak relative power output was also significantl

224 In the presence of NEM-S1, the rate and amplitude of the caged ADP response

225 n with wild-type troponin in the presence of NEM-S1.

226 to 5.52+/-0.02 pCa units in the presence of NEM-S1.

227 However, the operating principles of NEM switches and semiconductor switches are fundamentall

228 uffers containing excess molar quantities of NEM compared with samples homogenized in MeOH containing

229 scale manufacture of a representative set of NEM-based devices.

230 To further localize the site of NEM action, we mutated three cysteine residues in the C

231 -33 and Cys-273 in hCAT-2A as the targets of NEM inhibition.

232 Extensive washout of NEM-S1 from the treated fibres restored the low-velocity

233 The inhibition of either CcO or NEM-CcO with potassium cyanide prevented detectable MNP

234 ches with MTS-ethyltrimethylamine (MTSET) or NEM dramatically potentiated the channel's response to b

235 Hence, in accord with the previous proposal, NEM-FTR is shown to be a stable analogue of a one-electr

236 We found that CaM overexpression reduced NEM augmentation of KCNQ2, KCNQ4, and KCNQ5, and NEM pre

237 More specifically, NEM increased the phosphorylation of serine 940 (Ser-940

238 structures of Ssa1p and NEM-modified Ssa1p (NEM-Ssa1p) were compared using a variety of biophysical

239 easurements of core complexes confirmed that NEM caused an increase in the levels of SNARE core compl

240 Together, these results demonstrate that NEM alters the conformation of Ssa1p and disrupts, but d

241 Our results also demonstrated that NEM treatment of PC12 cells enhanced the dephosphorylati

242 in alkylating protein thiols and found that NEM required less reagent (125 vs. 1000 mol:mol excess),

243 ction fluorescence microscopy indicated that NEM action is not caused by increased trafficking of cha

244 ment of the thermal stability indicated that NEM modification has an effect very similar to that of b

245 e to the sulfhydryl reagent, indicating that NEM inhibition results from alkylation of Cys122.

246 sion in the plasma membrane, indicating that NEM reduces the intrinsic transporter activity.

247 ly reactive cG58C substitution revealed that NEM modification of a single c subunit in the oligomeric

248 Size exclusion chromatography revealed that NEM-Ssa1p is more oligomeric and more resistant to nucle

249 erse transcription intermediates showed that NEM and 2,2'-dipyridyl disulfide (aldrithiol-2), a reage

250 These results suggest that NEM enhances Ncd binding to MTs by disruption of neck an

251 of the augmentation by NEM, suggesting that NEM acts via alkylation of this residue.

252 The NEM alkylating reagent was critical in minimizing disulf

253 The NEM consistently achieved higher islet yields from pancr

254 The NEM was first tested in split pancreas (n=5) experiments

255 fect the ATPase activity were altered in the NEM conjugated N508C isoform.

256 In autologous isolation, the NEM yielded more than 200,000 IEQ from 19 of 21 pancreas

257 ties are also demonstrated by monitoring the NEM modification stoichiometries by electrospray mass sp

258 MALDI analysis of the NEM-inactivated enzyme showed Cys25 as the site of alkyl

259 Reaction of the NEM-treated enzyme with 6-BDB-[32P]TAMP results in 2 mol

260 The findings demonstrate that the NEM-sensitive face of helix II participates in ligand-in

261 activation was rapid and proportional to the NEM concentration.

262 a possible connection of this region to the NEM- and Ag+-sensitive region of TMH4 described previous

263 Using the NEM, islet products met release criteria for transplanta

264 When the NEM-modified HbA is also subjected to enzymatic treatmen

265 double mutant C33A/C273A was insensitive to NEM inhibition, whereas reintroduction of a cysteine at

266 onserved in all CAT isoforms did not lead to NEM insensitivity of hCAT-2A.

267 33 or 273 in the cysteine-less mutant led to NEM sensitivity.

268 binding are unrelated to RyR activity or to NEM alkylation of RyRs.

269 n-sulfhydryl reagent structurally related to NEM, N-ethylsuccinimide (0.1-0.5 mm), also elicited SR C

270 Cys-less permease is completely resistant to NEM inhibition.

271 This differential sensitivity to NEM alkylation suggests that in the adult rat striatum,

272 We thus wondered if sensitivity to NEM distinguishes generally all CAT and y(+)LAT isoforms

273 RpoS or Dps had an increased sensitivity to NEM in both exponential- and stationary-phase cells comp

274 ystems displayed even greater sensitivity to NEM.

275 EM are accessible to MTSES; however, the two NEM-reactive mutants at the cytoplasmic end of helix VII

276 Using NEM for thiol alkylation, DTT for disulfide reduction, a

277 reactive thiols and the TNB anion, and using NEM, four of the six reactive thiols are critical to the

278 nterdomain coupling and to determine whether NEM alters Ssa1p's conformation, the structures of Ssa1p

279 To investigate the mechanism by which NEM inhibits Ncd, the recombinant Ncd motor-stalk protei

280 When the cysteine residues are blocked with NEM, one or more tyrosine residues become the preferred

281 was faster and exhibited less curvature with NEM-S1.

282 Here, 1-3 log(1)(0) kill was found with NEM cysts for three of four MPDSs compared with one of f

283 roxide system gave 1-1.9 log(1)(0) kill with NEM cysts and 0.8-1.1 for NNA cysts.

284 n in the helix, only five mutants label with NEM.

285 se, most likely by an interaction of NO with NEM rather than an inactivation of RyRs by NO.

286 capsids isolated from cells pretreated with NEM did not.

287 Pretreatment with NEM occluded NO activation.

288 w that most of the positions that react with NEM are accessible to MTSES; however, the two NEM-reacti

289 ytoplasmic halves of both helices react with NEM in the absence of ligand, while Cys residues in the

290 321, 324, 328, 332, or 333 do not react with NEM under the conditions tested.

291 ese cysteines by oxidation and reaction with NEM (N-ethylmaleimide).

292 After treatment of seHAS with NEM, the V(max) value was decreased approximately 50%, a

293 Treatment of slices with NEM for up to 1 h, either in the presence or the absence

294 Treatment with NEM caused inactivation of wild-type hBAT.

295 exposed to 1:1 PHMB prior to treatment with NEM or IAM.

296 RBCs and stimulation in RBCs untreated with NEM.

297 nc fingers, we treated infectious virus with NEM and evaluated inactivation of infectivity in cell-ba

298 ted so that force was equal with and without NEM-S1, myocyte shortening was faster and exhibited less

299 d NaCl (WPI+NaCl), 5mM N-ethylmaleimide (WPI+NEM) or 20mM added NaCl and 5mM NEM (WPI+NaCl+NEM).

300 ctions between proteins, than the heated WPI+NEM and WPI+NaCl+NEM solutions.