ライフサイエンスコーパス: methanethiosulfonate

1 thyl methanethiosulfonate and ethylsulfonate methanethiosulfonate).

2 aut's reagent) and MTS1 [1,1-methanediyl bis(methanethiosulfonate)].

3 e was fully restored by adding ethylammonium methanethiosulfonate.

4 SEA-biotin) and [2-(trimethylammonium)ethyl] methanethiosulfonate.

5 either a biotin- or Texas red-derivative of methanethiosulfonate.

6 methanethiosulfonate and (2-sulfonatoethyl) methanethiosulfonate.

7 y quinacrine from reaction with 2-aminoethyl methanethiosulfonate.

8 thiol-specific agent ethyltrimethylammonium methanethiosulfonate.

9 t had been treated with N-biotinylaminoethyl methanethiosulfonate.

10 hanethiosulfonate and ethyltrimethylammonium methanethiosulfonate.

11 e Cys-directed reagent, N-biotinylaminoethyl methanethiosulfonate.

12 rd the impermeant 2-(trimethylammonium)ethyl methanethiosulfonate.

13 to the polar sulfhydryl reagent 2-aminoethyl methanethiosulfonate.

14 sensitive to the inhibition by (2-aminoethyl)methanethiosulfonate.

15 ne residues with impermeant 2-sulfonatoethyl methanethiosulfonate.

16 -impermeant probe 2-(trimethylammonium)ethyl methanethiosulfonate.

17 wo cysteines to modification by 2-aminoethyl methanethiosulfonate.

18 (TM) 6 as the residue responsible for methyl methanethiosulfonate (a membrane-permeable sulfhydryl mo

19 tants were labeled with N-biotinylaminoethyl methanethiosulfonate, a membrane-impermeable cysteine-di

20 (1-oxy-2,2,5,5-tetramethylpyrroline-3-methyl)methanethiosulfonate, a spin label reagent, were studied

21 tion of Cys201 was further demonstrated with methanethiosulfonate, a spin-labeled probe.

22 Treatment with 2-([biotinoyl] amino) ethyl methanethiosulfonate, a thiol-specific reagent that reac

23 ively large molecule [2-(trimethylammonium)] methanethiosulfonate accessed positions near the putativ

24 onist 2-nonanone protected the receptor from methanethiosulfonate action at position 148, placing thi

25 Exposure to methanethiosulfonate agents that modify cysteine residue

26 inactivation by [2-(trimethylammonium)ethyl] methanethiosulfonate and (2-sulfonatoethyl) methanethios

27 active methanethiosulfonates [sulforhodamine-methanethiosulfonate and 2-((biotinoyl)amino)ethyl metha

28 bited by thiol-specific agents (carboxyethyl methanethiosulfonate and ethylsulfonate methanethiosulfo

29 Added study with carboxyethyl methanethiosulfonate and ethylsulfonate methylthiosulfon

30 meant, thiol-specific reagents, carboxyethyl methanethiosulfonate and ethyltrimethylammonium methanet

31 n 172, which reacted with both (2-aminoethyl)methanethiosulfonate and N-biotinylaminoethyl methanethi

32 ifunctional cross-linker 1,3-propanediyl bis-methanethiosulfonate and Western blotting, hRFC species

33 f this residue to 2-(trimethylammonium)ethyl methanethiosulfonate, and the bumetanide insensitivity o

34 Y102C was accessible to modification by methanethiosulfonate, and this modification was prevente

35 ing were also modified by 1 mm (2-aminoethyl)methanethiosulfonate applied in the absence of ATP when

36 ssays with membrane-impermeable 2-aminoethyl methanethiosulfonate-biotin and streptavidin beads to de

37 TMD2-3 loop domain reacted with 2-aminoethyl methanethiosulfonate-biotin, establishing aqueous access

38 nit c and tested for cross-linking using bis-methanethiosulfonate (bis-MTS) reagents.

39 reactive reagent 2-(trimethylammonium)ethyl methanethiosulfonate bromide (MTSET) alters in a phospho

40 block by inside [2-(trimethylammonium)ethyl]methanethiosulfonate bromide (MTSET) at slow stimulation

41 ere sensitive to [2-(trimethylammonium)ethyl]methanethiosulfonate bromide (MTSET) or MTSEA.

42 ide (MTSEA) and [(2-(trimethylammonium)ethyl]methanethiosulfonate bromide (MTSET)) and to Cd(2+) was

43 eactive reagent [2-(trimethylammonium)ethyl] methanethiosulfonate bromide (MTSET), alpha-beta-gamma H

44 fonate (MTSEA), [2-(trimethylammonium) ethyl]methanethiosulfonate bromide (MTSET), and sodium (2-sulf

45 modification by [2-(trimethylammonium)ethyl]methanethiosulfonate bromide (MTSET), channels exhibited

46 MTSEA) or 1 mM [2-(trimethylammonium) ethyl] methanethiosulfonate bromide (MTSET).

47 g site, because [2-(trimethylammonium)ethyl] methanethiosulfonate bromide did not prevent zinc potent

48 accessibility to 2-[(trimethylammonium)ethyl]methanethiosulfonate bromide modification were observed

49 modification by (2-(trimethylammonium)ethyl) methanethiosulfonate bromide of Cys at position 79 impac

50 n response to [(2-(trimethylammonium) ethyl] methanethiosulfonate bromide, or with brefeldin A, sugge

51 -active reagent [2-(trimethylammonium)ethyl] methanethiosulfonate bromide.

52 ubstrate analog [2-(trimethylammonium)-ethyl]methanethiosulfonate but was inaccessible to tetramethyl

53 hydryl modification of Y124C by 2-aminoethyl methanethiosulfonate, but not by N-ethylmaleimide, was f

54 s to the negatively charged 2-sulfonatoethyl methanethiosulfonate, but not neutral 2-hydroxyethyl met

55 tion, whereas [2-(trimethyl ammonium) ethyl] methanethiosulfonate chloride modification of I521C in t

56 in Xenopus oocytes and the current block by methanethiosulfonate compounds was measured.

57 ate the general utility of the 4-thiouridine/methanethiosulfonate coupling method to introduce nitrox

58 hetic propanethiol, or alternatively, propyl methanethiosulfonate, covalently binds to cysteine resid

59 anethiosulfonate, or 2-trimethylammonioethyl methanethiosulfonate, decreased the glycine EC(50) to re

60 ced cysteine residues to sulfhydryl-reactive methanethiosulfonate derivatives ((2-aminoethyl)methanet

61 eaction of Cys-90 or Cys-306 with impermeant methanethiosulfonate derivatives enhanced dopamine uptak

62 ed sulfhydryl group with membrane-impermeant methanethiosulfonate derivatives inhibited substrate tra

63 reated with hydrophilic, sulfhydryl-specific methanethiosulfonate derivatives with control cell membr

64 brane domain three followed by labeling with methanethiosulfonate derivatives.

65 single and combination cysteine mutants with methanethiosulfonate ethylamine revealed that [(3)H]dihy

66 hen proteoliposomes were treated with MTSEA (methanethiosulfonate ethylamine), a thiol-specific reage

67 of Cys(439) by a 10,000-fold molar excess of methanethiosulfonate ethylamine, demonstrating that Cys(

68 logous mutation in NR2A, -2B, -2C, or -2D by methanethiosulfonate ethylammonium (MT-SEA) occurs only

69 the hydrophilic sulfhydryl-modifying agents methanethiosulfonate ethylammonium (MTSEA(+)) and methan

70 ssible in the binding-site crevice by use of methanethiosulfonate ethylammonium (MTSEA) and inferred

71 8, a piperidinyl antagonist, is inhibited by methanethiosulfonate ethylammonium (MTSEA) in a time- an

72 ositions tested, the presence of ACh changed methanethiosulfonate ethylammonium (MTSEA) modification

73 respectively, were found to be accessible to methanethiosulfonate ethylammonium (MTSEA) or methanethi

74 was diminished by chemical modification with methanethiosulfonate ethylammonium (MTSEA) to the outer

75 plication of the cysteine modification agent methanethiosulfonate ethylammonium (MTSEA) to V787C demo

76 hanethiosulfonate ethylsulfonate (MTSES) and methanethiosulfonate ethylammonium (MTSEA)) did not affe

77 charged, hydrophilic, thiol-specific reagent methanethiosulfonate ethylammonium (MTSEA), [(3)H]CP5594

78 delta receptor was relatively insensitive to methanethiosulfonate ethylammonium (MTSEA), a positively

79 hin the protein that binds membrane-permeant methanethiosulfonate ethylammonium (MTSEA), but not memb

80 s of introduced cysteines to modification by methanethiosulfonate ethylammonium (MTSEA)-Biotin were m

81 o not externally accessible when probed with methanethiosulfonate ethylammonium (MTSEA).

82 Previously we showed that methanethiosulfonate ethylammonium (MTSEA+) covalently m

83 sitively charged sulfhydryl-specific reagent methanethiosulfonate ethylammonium reacted with a cystei

84 by the sulfhydryl-specific modifying reagent methanethiosulfonate ethylammonium.

85 hanges when the sulphydryl modifying reagent methanethiosulfonate-ethylammonium (MTSEA) was applied.

86 nethiosulfonate ethylammonium (MTSEA(+)) and methanethiosulfonate ethylsulfonate (MTSES(-)) on wild-t

87 channels with methanethiosulfonate reagents (methanethiosulfonate ethylsulfonate (MTSES) and methanet

88 Labeling studies with methanethiosulfonate ethylsulfonate (MTSES) show that po

89 g loops, with N-[14C]ethylmaleimide (NEM) or methanethiosulfonate ethylsulfonate (MTSES) was studied

90 c reagents N-[(14)C]ethylmaleimide (NEM) and methanethiosulfonate ethylsulfonate (MTSES) which are pe

91 Studies with methanethiosulfonate ethylsulfonate (MTSES), a hydrophil

92 h membrane-impermeant thiol reagents such as methanethiosulfonate ethylsulfonate (MTSES).

93 sulfonate ethyltrimethylammonium (MTSET) and methanethiosulfonate ethylsulfonate (MTSES).

94 nium)ethyl]methanethiosulfonate (MTSET), and methanethiosulfonate ethylsulfonate (MTSES)] of mutants

95 Studies with methanethiosulfonate ethylsulfonate indicate that Cys re

96 storing the negative charge at position 518 (methanethiosulfonate ethylsulfonate modification of 518C

97 Methanethiosulfonate ethylsulfonate, an impermeant thiol

98 ionally, the smaller thiol-reactive reagent, methanethiosulfonate ethylsulfonate, reduced transport b

99 mmonium (MTSEA), but not membrane-impermeant methanethiosulfonate ethyltrimethylammonium (MTSET) and

100 ethanethiosulfonate ethylammonium (MTSEA) or methanethiosulfonate ethyltrimethylammonium (MTSET) and

101 Extracellular treatment with methanethiosulfonate ethyltrimethylammonium (MTSET) of a

102 .1 outer pore from permanent modification by methanethiosulfonate ethyltrimethylammonium (MTSET).

103 f the membrane-impermeant sulfhydryl reagent methanethiosulfonate ethyltrimethylammonium with the ext

104 ammonium pharmacophore of the agonist analog methanethiosulfonate-ethyltrimethylammonium would be in

105 beling by MTSET {[2-(trimethylammonium)ethyl]methanethiosulfonate} from both the cytoplasmic and extr

106 hanethiosulfonate derivatives ((2-aminoethyl)methanethiosulfonate hydrobromide (MTSEA) and [(2-(trime

107 2-(Aminoethyl)methanethiosulfonate hydrobromide (MTSEA) failed to inhi

108 le to both outside and inside 2-(aminoethyl)-methanethiosulfonate hydrobromide (MTSEA) Further study

109 inding by the cysteine reagent 2-(aminoethyl)methanethiosulfonate hydrobromide (MTSEA) in membrane pr

110 sured in the presence of 2.5 mM 2-aminoethyl methanethiosulfonate hydrobromide (MTSEA) or 1 mM [2-(tr

111 2-(Aminoethyl)-methanethiosulfonate hydrobromide (MTSEA)-biotin labeled

112 ently covalently modified with (2-aminoethyl)methanethiosulfonate hydrobromide, a reagent that restor

113 substituted for D43 and T47) by 2-aminoethyl methanethiosulfonate in the GABAA alpha1 subunit loop G

114 sulfhydryl-specific chemical cross-linkers, methanethiosulfonates, inactivated the AcrB transporter

115 -reactive reagent 2-(trimethylammonium)ethyl methanethiosulfonate, indicating the location of candida

116 Exposure to ethylammonium methanethiosulfonate inhibited acetylcholine-induced cur

117 with the cysteine protease inhibitor, methyl methanethiosulfonate, inhibited both cleavage and enzyma

118 Propyl methanethiosulfonate is an anesthetic analog that covale

119 ved when the smaller labeling reagent methyl methanethiosulfonate is employed, suggesting that it ref

120 ET) method employing a novel, nonfluorescent methanethiosulfonate-linked acceptor that can be reversi

121 full inhibition of S359C by the impermeable methanethiosulfonate-linked probes must reflect an appro

122 this study, the reactivity between S-methyl methanethiosulfonate (MMTS) with persulfide was unambigu

123 The accessibility of Y67C to methanethiosulfonate modification indicated that its sid

124 vation of the receptor increased the rate of methanethiosulfonate modification of alpha(1)D62C and al

125 gamma-Aminobutyric acid (GABA) slowed methanethiosulfonate modification of alpha(1)F64C, alpha

126 [2-(Trimethylammonium)-ethyl]methanethiosulfonate modification of Cys-478 blocked sub

127 nd pentobarbital slowed N-biotinylaminoethyl methanethiosulfonate modification of T160C and D163C, in

128 the strongest influence on conductance from methanethiosulfonate modification, while leaving the sit

129 N-Biotinylaminoethyl methanethiosulfonate modified P174C-, R176C-, S177C-, V1

130 performed cysteine-scanning mutagenesis and methanethiosulfonate (MTS) accessibility studies on thes

131 P2X2(I328C) receptor was activated by propyl-methanethiosulfonate (MTS) as effectively as by ATP, but

132 The ability of sulfhydryl-specific alkyl methanethiosulfonate (MTS) compounds of different length

133 mutant receptors can be regulated by charged methanethiosulfonate (MTS) compounds.

134 delta, and kappa opioid receptors to charged methanethiosulfonate (MTS) derivatives and identified th

135 With regard to methanethiosulfonate (MTS) inactivation of uptake, TM6a

136 The present study characterizes the methanethiosulfonate (MTS) inhibition profiles of 26 con

137 er (hSERT) proteins, we utilized the largely methanethiosulfonate (MTS) insensitive hSERT C109A mutan

138 ore rapidly modified by a negatively charged methanethiosulfonate (MTS) reagent, 2-sulfonatoethyl MTS

139 residues in subunit a with cysteine reactive methanethiosulfonate (MTS) reagents and Cd(2+).

140 Cytoplasmic-side methanethiosulfonate (MTS) reagents blocked K(+) permeat

141 positions (E54C/D58C) and tested a series of methanethiosulfonate (MTS) reagents for their effects on

142 We demonstrate that methanethiosulfonate (MTS) reagents form disulfide bonds

143 Here, we investigated CFTR's TM1 by applying methanethiosulfonate (MTS) reagents from both cytoplasmi

144 ere recorded before and after application of methanethiosulfonate (MTS) reagents in the resting, GABA

145 Intracellular application of certain charged methanethiosulfonate (MTS) reagents modified and irrever

146 Here we probed the reactivity toward methanethiosulfonate (MTS) reagents of channels with cys

147 rg(436) with Cys and examining the effect of methanethiosulfonate (MTS) reagents on gamma.

148 five predicted internal loops, reacted with methanethiosulfonate (MTS) reagents only when the plasma

149 Tethering thiol-reactive methanethiosulfonate (MTS) reagents onto alpha1K219C, be

150 Small, cysteine-specific methanethiosulfonate (MTS) reagents reacted with four TM

151 ccessibility mutagenesis and thiol-modifying methanethiosulfonate (MTS) reagents to further probe the

152 Methanethiosulfonate (MTS) reagents were used to modify

153 respectively, to inhibition by all the three methanethiosulfonate (MTS) reagents, I441C had >50% sens

154 2.59S which is relatively insensitive to the methanethiosulfonate (MTS) reagents, we mutated to cyste

155 re assayed for inhibition by thiol-reactive, methanethiosulfonate (MTS) reagents.

156 nd extracellularly placed positively charged methanethiosulfonate (MTS) reagents.

157 e extracellular side of M2, were modified by methanethiosulfonate (MTS) reagents.

158 end of the first transmembrane segment, with methanethiosulfonate (MTS) reagents.

159 agenesis and hydrophilic sulfhydryl-reactive methanethiosulfonate (MTS) reagents.

160 cessible to hydrophilic, membrane-impermeant methanethiosulfonate (MTS) reagents.

161 extracellularly and intracellularly applied methanethiosulfonate (MTS) reagents.

162 e permeation pathway that were reactive with methanethiosulfonate (MTS) reagents.

163 elix seven, C386 (C7.42), is reactive toward methanethiosulfonate (MTS) sulfhydryl labeling agents, a

164 before and after treatment with a variety of methanethiosulfonate (MTS)-based compounds, using voltag

165 secutive amino acids was performed against a methanethiosulfonate (MTS)-resistant background (C270A).

166 the sulfhydryl reagent, N-biotinylaminoethyl methanethiosulfonate (MTS).

167 ted cysteine to modification by 2-aminoethyl methanethiosulfonate (MTS-EA) in excised macropatches.

168 6)-tetramethylrhodamine)carboxylamino) ethyl methanethiosulfonate (MTS-TAMRA) cysteine-reactive reage

169 6)-tetramethylrhodamine)carboxylamino) ethyl methanethiosulfonate (MTS-TAMRA) revealed Thr-442 marks

170 (6)-tetramethylrhodamine)carboxylamino)ethyl methanethiosulfonate (MTS-TAMRA)) sulfhydryl reagents, 4

171 Methanethiosulfonates (MTS) are known to inactivate the

172 Membrane-impermeant methanethiosulfonates (MTS) inhibited bile acid transpor

173 Disulfide, bis(methanethiosulfonate) (MTS), and dibromobimane (DBB) cro

174 2-Aminoethyl methanethiosulfonate (MTSEA(+)) failed to modify Cd(2+)-

175 tion by the sulfhydryl reagents 2-aminoethyl methanethiosulfonate (MTSEA) and 2-(trimethylammonium)et

176 Pretreatment with (2-aminoethyl)methanethiosulfonate (MTSEA) inhibited [(3)H]diprenorphi

177 reased the rate of reaction of (2-aminoethyl)methanethiosulfonate (MTSEA) with X-A342C, the construct

178 ity to polar MTS derivatives [(2-aminoethyl)-methanethiosulfonate (MTSEA), [2-(trimethylammonium)ethy

179 ntrast, the smaller compound, 2-(aminoethyl) methanethiosulfonate (MTSEA), modified a position predic

180 rachloromercuribenzoic acid and 2-aminoethyl methanethiosulfonate (MTSEA), which share with ONOO(-) t

181 anethiosulfonate (MTSET), and (2-aminoethyl) methanethiosulfonate (MTSEA).

182 thiosulfonate reagents N-biotinoylaminoethyl methanethiosulfonate (MTSEA-biotin) and [2-(trimethylamm

183 the thiol oxidant 2-((biotinoyl)amino)ethyl methanethiosulfonate (MTSEA-biotin) and that electrophil

184 data received from the N-biotinylaminoethyl methanethiosulfonate (MTSEA-biotin) labeling of SERT on

185 N-biotinylaminoethyl methanethiosulfonate (MTSEA-biotin) reacts with cysteine

186 hydryl-specific reagent N-biotinylaminoethyl methanethiosulfonate (MTSEA-Biotin) was used to covalent

187 Treatment with sodium (2-sulfonatoethyl) methanethiosulfonate (MTSES) had no effect on hRFC activ

188 ibition mediated by sodium (2-sulfonatoethyl)methanethiosulfonate (MTSES) indicated that citrate conf

189 le, thiol-reactive anion Na(2-sulfonatoethyl)methanethiosulfonate (MTSES) into the substrate pathway,

190 Two probes, the large [2-sulfonatoethyl]methanethiosulfonate (MTSES) molecule and permeant Au(CN

191 ification of the site with (2-sulfonatoethyl)methanethiosulfonate (MTSES) results in an enhanced resp

192 omide (MTSET), and sodium (2-sulfonatoethyl)-methanethiosulfonate (MTSES) similarly and profoundly in

193 on of the Y126C mutant by (2-sulfonatoethyl) methanethiosulfonate (MTSES)) hRFC monomers were express

194 anethiosulfonate reagents (2-sulfonatoethyl) methanethiosulfonate (MTSES), [2-(trimethylammonium)ethy

195 hiol-reactive anion sodium (2-sulfonatoethyl)methanethiosulfonate (MTSES), and the requirement for a

196 cysteine-specific reagent (2-sulfonatoethyl) methanethiosulfonate (MTSES), but only K84C was sensitiv

197 In addition, sodium (2-sulfonatoethyl) methanethiosulfonate (MTSES), used to irreversibly bind

198 methods (SCAM) with sodium (2-sulfonatoethyl)methanethiosulfonate (MTSES).

199 id) were both inhibited by (2-sulfonatoethyl)methanethiosulfonate (MTSES; 10-500 microm)-induced alka

200 ermeant reagent [2-(trimethylammonium)ethyl]-methanethiosulfonate (MTSET) and protected by substrate.

201 in HeLa cells by [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET) occurred much more readily

202 sition 380/449 by 2-(trimethylammonium)ethyl methanethiosulfonate (MTSET) proceeded at identical rate

203 permeant reagent [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET) to the replacement cysteine

204 with the reagent [2-(triethylammonium)ethyl]methanethiosulfonate (MTSET) which introduces five posit

205 lfonate (MTSES), [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET), and (2-aminoethyl) methane

206 bed with Hg(2+), [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET), and biotin-maleimide, appl

207 lfonate (MTSEA), [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET), and methanethiosulfonate e

208 ocytin (MPB) and [2-(trimethylammonium)ethyl]methanethiosulfonate (MTSET), have no effect.

209 [2-(Trimethylammonium)-ethyl]-methanethiosulfonate (MTSET), which attaches thiocholine

210 onate (MTSEA) and 2-(trimethylammonium)ethyl methanethiosulfonate (MTSET).

211 oreactive agent 2-((trimethylammonium)ethyl) methanethiosulfonate (MTSET).

212 modification by [2-(trimethylammonium)ethyl] methanethiosulfonate (MTSET+), which increases conductan

213 mechanism, we used the membrane-impermeable methanethiosulfonates, MTSET and MTS-TEAH, to modify Kir

214 2,5, 5-tetramethyl-Delta3-pyrroline-3-methyl)methanethiosulfonate (MTSL), we have introduced a nitrox

215 at of MTSEA(+) or 3-(triethylammonium)propyl methanethiosulfonate (MTSPTrEA(+)), implying that qBBr(+

216 were subsequently modified with one of three methanethiosulfonate nitroxide reagents to introduce a s

217 protection of Cys148 in lactose permease, a methanethiosulfonate nitroxide spin-label was directed s

218 ethanethiosulfonate and N-biotinylaminoethyl methanethiosulfonate on the surface of intact cells.

219 ning effects of sulfhydryl-modifying agents (methanethiosulfonates) on 20 cysteine-substituted mutant

220 of alphaM1, which reacted with 2-aminoethyl methanethiosulfonate only in the presence of ACh, reacte

221 iosulfonate, positively charged 2-aminoethyl methanethiosulfonate, or 2-trimethylammonioethyl methane

222 2,2,5,5-tetramethyl-3-pyrrolidin-3-yl)methyl methanethiosulfonate] placed at three locations in the t

223 hiosulfonate, but not neutral 2-hydroxyethyl methanethiosulfonate, positively charged 2-aminoethyl me

224 be selectively and irreversibly inhibited by methanethiosulfonates presumably through conjugation to

225 In addition, methanethiosulfonate reaction rates were fastest for alp

226 er supported by [2-(trimethylammonium)ethyl]-methanethiosulfonate reactivity on the DAT E2C I159C.

227 lf-inhibition responses and the effects of a methanethiosulfonate reagent on channel currents in sing

228 ile cross-linking reaction of a bifunctional methanethiosulfonate reagent with pairs of cysteine resi

229 ng of M2 positions with an alcohol analog, a methanethiosulfonate reagent, further implicated residue

230 ion of intact cells with a novel fluorescent methanethiosulfonate reagent.

231 idues toward N-ethyl maleimide and a charged methanethiosulfonate reagent.

232 448 were tested for their sensitivity to the methanethiosulfonate reagents (2-sulfonatoethyl) methane

233 on of the cysteine-substituted channels with methanethiosulfonate reagents (methanethiosulfonate ethy

234 utated to cysteines and their sensitivity to methanethiosulfonate reagents (MTS) was tested.

235 N-Ethylmaleimide or derivatized methanethiosulfonate reagents (neutral or charged) were

236 nctional channel differentially sensitive to methanethiosulfonate reagents and cadmium, suggested tha

237 tituted cysteines to extracellularly applied methanethiosulfonate reagents and the rates of their mod

238 Positively charged methanethiosulfonate reagents derivatized alpha(1)F64C a

239 ltered the rates of cysteine modification by methanethiosulfonate reagents differently than GABA.

240 ation rate of these substituted cysteines by methanethiosulfonate reagents either in the presence or

241 ludes amiloride as well as anionic and large methanethiosulfonate reagents from the pore.

242 Methanethiosulfonate reagents inhibited the activity of

243 open state, but Ag+ and sulfhydryl-specific methanethiosulfonate reagents modified the channels with

244 of zinc potentiation upon treatment with the methanethiosulfonate reagents N-biotinoylaminoethyl meth

245 Methanethiosulfonate reagents of different size and char

246 ACh increased the inhibition by methanethiosulfonate reagents of N170C and did not chang

247 Tethering chemically diverse thiol-reactive methanethiosulfonate reagents onto alpha(1)K219C and alp

248 Reaction with several methanethiosulfonate reagents potentiated currents to wi

249 Methanethiosulfonate reagents reacted with alpha(1)T60C,

250 ies of accessibility with positively charged methanethiosulfonate reagents suggest that the permeatio

251 bility of three hydrophilic, thiol reactive, methanethiosulfonate reagents to a library of 21 single-

252 ccessibility of hydrophilic, thiol-reactive, methanethiosulfonate reagents to a library of 68 indepen

253 eated with Cu(2+) ions or with bi-functional methanethiosulfonate reagents to catalyze cross-link for

254 ave been modified with a series of nitroxide methanethiosulfonate reagents to investigate the structu

255 cessibility of each single Cys mutant to two methanethiosulfonate reagents was evaluated by determini

256 ssibility of each single Cys mutant to three methanethiosulfonate reagents was evaluated by determini

257 Sensitivity to N-ethylmaleimide (NEM) and methanethiosulfonate reagents was localized to a membran

258 bited by incubation with sulfhydryl-specific methanethiosulfonate reagents, denoting their solvent ac

259 rt protein to hydrophilic, cysteine-specific methanethiosulfonate reagents, enabled identification of

260 in accessibility of substituted cysteines to methanethiosulfonate reagents.

261 t those two positions with variously charged methanethiosulfonate reagents.

262 utants in transmembrane domains 3 and 4 with methanethiosulfonate reagents.

263 ying the cysteine side chain with reversible methanethiosulfonate reagents.

264 the membrane-impermeant, sulfhydryl-specific methanethiosulfonate reagents.

265 of wild type (WT) and E53C GlyRs exposed to methanethiosulfonate reagents.

266 agents tested, including membrane impermeant methanethiosulfonate reagents.

267 hanol as well as reagents: mixed disulfides (methanethiosulfonate reagents: MTSET+, MTSES-) and an al

268 ethiosulfonate and 2-((biotinoyl)amino)ethyl methanethiosulfonate] reduced both ATP-evoked currents a

269 f alphaY198C by [3-(trimethylammonium)propyl]methanethiosulfonate resulted in irreversible activation

270 CFTR channels by [2-(trimethylammonium)ethyl]methanethiosulfonate resulted in the simultaneous modifi

271 itions tested) by [(trimethylammonium)methyl]methanethiosulfonate resulted only in irreversible inhib

272 However, propyl methanethiosulfonate reversibly inhibited cysteine-subst

273 hermore, labeling with N-biotinoylaminoethyl methanethiosulfonate showed that I66C was weakly reactiv

274 a negatively charged group [2-sulfonatoethyl methanethiosulfonate sodium salt (MTSES)] rescued the cG

275 find that the thiol modifying reagent methyl methanethiosulfonate specifically inhibits NO activation

276 the behavior of CM15 analogs labeled with a methanethiosulfonate spin label (MTSL) and a brominated

277 We find that the methanethiosulfonate spin label can occasionally induce

278 in fusion peptide that has been labeled with methanethiosulfonate spin label.

279 -oxyl-2,2,5,5-tetramethylpyrroline-3-methyl)-methanethiosulfonate spin labels (MTSSL) bound to CaM mu

280 lysozyme (T4L) mutants, doubly labeled with methanethiosulfonate spin-label (MTSSL), have been studi

281 -resolution structures were obtained for the methanethiosulfonate spin-label derivatized to cysteines

282 ed the cysteine with the sulfhydryl-specific methanethiosulfonate spin-label, and used electron param

283 hree Ca(2+)-binding loops and labeled with a methanethiosulfonate spin-label.

284 tants of motifs II and III are accessible to methanethiosulfonates, suggesting that these segments ex

285 cient PK15 cells and probed with a series of methanethiosulfonate sulfhydryl-modifying reagents.

286 Furthermore, larger cysteine-reactive methanethiosulfonates [sulforhodamine-methanethiosulfona

287 te and the covalent attachment of benzocaine-methanethiosulfonate to a cysteine introduced in the ext

288 We also applied [2-(triethylammonium)ethyl] methanethiosulfonate to covalently modify the introduced

289 ility and reaction rate of propyl- and hexyl-methanethiosulfonate to cysteine residues introduced int

290 d MTSEA-biotinylation (N-Biotinoylaminoethyl methanethiosulfonate) to show ATP-sensitive accessibilit

291 Mutagenesis and methanethiosulfonate treatment are less effective at pos

292 Mutagenesis and methanethiosulfonate treatment are most effective at pos

293 brane-impermeant [2-(trimethylammonium)ethyl]methanethiosulfonate was able to access the inner pore f

294 ein showed that inhibition by ethylsulfonate methanethiosulfonate was blocked by substrate and that t

295 lly, 2-[(5-fluoresceinyl)aminocarbonyl]ethyl methanethiosulfonate was conjugated to a free cysteine o

296 the amount of inactivation by (2-aminoethyl)methanethiosulfonate was less than expected if the two f

297 ccess alkylator, 2-[(trimethylammonium)ethyl]methanethiosulfonate, was not effective in unmasking the

298 larly and intracellularly added 2-aminoethyl methanethiosulfonate, we previously located the closed g

299 of reduced PDI by N-ethylmaleimide or methyl-methanethiosulfonate, which abolished PDI oxidoreductase

300 dryl-specific, charged reagent, 2-aminoethyl methanethiosulfonate with cysteines substituted for resi