ライフサイエンスコーパス: DIDS

1 DIDS (0.2 mmol/L) was used to block Ca(2+)-activated chl

2 DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid

3 DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic aci

4 DIDS and NPPB abolished the increase of duodenal bicarbo

5 DIDS at 100 micromol/L, a concentration at which DIDS is

6 DIDS blocked the alkaline response and revealed a prolon

7 DIDS crosslinks AQP1 monomers expressed in Pichia pastor

8 DIDS decreased basal pH(i), whereas NPPB increased pH(i)

9 DIDS has no effect on luminal alkalinization caused by t

10 DIDS is a commonly used anion channel antagonist that is

11 DIDS reduced baseline pH(i).

12 DIDS, a blocker of some KCC cotransporters and Cl(-)/HCO

13 DIDS-inhibitable mechanisms, possibly including HCO3-Cl

14 H(2)DIDS added to IOVs does not prevent cleavage at K743; th

15 ted reduction in intracellular Cl(-), as H(2)DIDS and removal of HCO(3)(-)/CO(2) inhibited the negati

16 ed modification of E681 or inhibition by H(2)DIDS are consistent with the idea that the new Cl(-) bin

17 cyanatodihydrostilbene-2,2'-disulfonate (H(2)DIDS), acting from the extracellular side, blocks trypsi

18 xchanger (AE) to produce HCO3- efflux, and a DIDS-insensitive Cl--OH- exchanger (CHE) to produce OH-

19 partly from astrocytes and is mediated by a DIDS-sensitive mechanism.

20 results are consistent with activation of a DIDS-sensitive Cl--HCO3- anion exchanger (AE) to produce

21 ters, including 13 transmembrane segments, a DIDS (4,4-diiodothiocyanatostilbene-2, 2-disulfonic acid

22 gest that *O(2)(-) exits endosomes through a DIDS-sensitive chloride channel(s) and that SOD1-mediate

23 iisothiocyanatostilbene-2,2'-disulfonic acid DIDS).

24 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and niflumic acid were evaluated for their ability

25 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and were not inhibited by phorbol esters or activa

26 iisothiocyanatostilbene-2,2'disulfonic acid (DIDS) inhibited Isc when added to either side of the bil

27 Diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) labeling of band 3, which is shown to shift most o

28 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) or 5-nitro-2-(3-phenylpropylamino) benzoic acid (N

29 iisothiocyano-2,2-stillbene-disulfonic acid (DIDS) reduced the frequency and blocked slow waves in mu

30 isothiocyanatostilbene-2,2'-disulfonic acid (DIDS), 5-nitro2-(3-phenylpropylamino)benzoic acid (NPPB)

31 cyanatodihydrostilbene-2,2'-disulfonic acid (DIDS), an anion exchange inhibitor, on the apical side p

32 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), and niflumic acid (NFA) in excised inside-out and

33 -diisothiocyanostilbene-2,2'disulfonic acid (DIDS), as well as by other bile acids.

34 iisothiocyanatostilbene-2,2'disulfonic acid (DIDS), attenuated the effects of CFTR on acceleration an

35 isothiocyanatostilbene-2,2'-disulfonic acid (DIDS), or diethylpyrocarbonate (DEPC).

36 isothiocyanatostilbene-2,2'-disulfonic acid (DIDS), which has been shown to block P2Y(2) receptors in

37 isothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-dependent pH(i) recovery in melanoma cells, in res

38 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-insensitive mechanism.

39 sothiocyanato-stilbene-2,2'-disulfonic acid (DIDS)-sensitive and gluconate-sensitive Cl(-) channels.

40 sothiocyanato-stilbene-2,2'-disulfonic acid (DIDS)-sensitive and Na(+)- and HCO(3)(-)-dependent (36)C

41 diisothiocyanostilbene-2,2'-disulfonic acid (DIDS).

42 diisothiocyanostilbene-2,2' disulfonic acid (DIDS).

43 sothiocyanatostilbene-2, 2'-disulfonic acid (DIDS).

44 isothiocyanatostilbene-2-2'-disulfonic acid (DIDS).

45 sothiocyanato-stilbene-2,2'-disulfonic acid (DIDS).

46 isothiocyanatostilbene-2,2'-disulfonic acid (DIDS).

47 sothiocyanatostilbene-2,2'-disulphonic acid (DIDS) and 4-acetamido-4'-isothiocyanatostilbene-2,2'-dis

48 isothiocyanostilbene-2, 2'-disulphonic acid (DIDS) and 4-acetamido-4'-isothiocyanostilbene-2, 2'-disu

49 othiocyanato-stilbene-2,2'-disulphonic acid (DIDS) application.

50 othiocyanato-stilbene-2,2'-disulphonic acid (DIDS) on Ca2+-activated Cl- current (I(Cl(Ca))) evoked b

51 sothiocyanatostilbene-2,2'-disulphonic acid (DIDS) partially inhibits luminal alkalinization caused b

52 iisothiocyanostilbene-2,2'-disulphonic acid (DIDS), also inhibited this current.

53 iisothiocyanostilbene-2,2'-disulphonic acid (DIDS), and was potentiated by inhibiting astrocytic conv

54 sothiocyanatostilbene-2,2'-disulphonic acid (DIDS), anthracene-9-carboxylate (9-AC) and niflumic acid

55 sothiocyanatostilbene-2,2'-disulphonic acid (DIDS), caused hyperpolarizations (10-15 mV) and dilatati

56 othiocyanatostilbene-2, 2'-disulphonic acid (DIDS).

57 othiocyanatostilbene-2, 2'-disulphonic acid (DIDS, 100 microM) also blocked the hypotonicity-induced

58 sothiocyanatostilbene-2,2'-disulphonic acid (DIDS; 100 microM) blocked RVD while 300 microM Cd2+ had

59 othiocyanatostilbene-2, 2'-disulphonic acid (DIDS; 200 microM), although the blockade by DIDS was vol

60 diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS) as a potent inhibitor of HCMV replication.

61 diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS) eliminated both the RVP and the persistent ECS shr

62 diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS), also blocked feedback.

63 diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS), an inhibitor of HCO3(-) uptake, had no effect on

64 diisothiocyanatostilbene-2,2'-sulfonic acid (DIDS), and complete enzyme inactivation was produced wit

65 diisothiocyano-2,2'-stilbenedisulfonic acid [DIDS]), its mechanism of action, and the chemical proper

66 sothiocyanatostilbene-2,2'-disulfonic acid), DIDS (4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid),

67 ty to block by glibenclamide, niflumic acid, DIDS and extracellular ATP.

68 ion through 24 hours treatment with ACSF +/- DIDS (40 or 400 microM).

69 uggest that intravascular pressure activates DIDS- and IAA-94-sensitive chloride channels to depolari

70 We observed that although DIDS induced echinocytic morphological changes in the tr

71 ratinocytes treated with 1,25(OH)(2)D(3) and DIDS at concentrations shown to block decreases in post-

72 ide channel blockers niflumic acid (81%) and DIDS (90%).

73 IAA-94 and DIDS had no effect on membrane potential or diameter of

74 Dilatations to IAA-94 and DIDS were unaffected by potassium channel blockers, but

75 Both acetazolamide and DIDS reduced chloride effluxes.

76 Ethacrynic acid and DIDS (4,4'-diisothiocyanato-stilbene-2,2'-disulfonic aci

77 lonic NBC is sensitive to both amiloride and DIDS.

78 A combination of bumetanide and DIDS decreased the response more than either drug alone.

79 D in T84 cells is the tamoxifen-, DDFSK- and DIDS-sensitive ICl(swell) and not the hyperpolarization-

80 ncing Na(+)-independent, Cl(-)-dependent and DIDS-sensitive HCO(3)(-) secretion, as monitored through

81 delta was 0.6 for A9C, 0.3 for DPC and DIDS, and <0.1 for NFA.

82 separate DIDS-sensitive/EIPA-insensitive and DIDS-insensitive/EIPA-sensitive NBC activities in both c

83 at positive voltages, sensitive to NPPB and DIDS, and inhibited by phorbol esters.

84 e treated with the AE2 transport antagonist, DIDS, we noted evidence for cross-linking of AE2 proteol

85 e hAQP1 by SDS-PAGE, reactivity with an anti-DIDS antibody shows that DIDS crosslinks hAQP1 monomers.

86 We also found that apical DIDS significantly inhibited the ATP-evoked [Ca2+]in and

87 Na of 7.3 and 4.3 mM, respectively; and are DIDS-sensitive with apparent Ki of 8.9 and 263.8 microM,

88 e with chloride transport inhibitors such as DIDS and niflumic acid.

89 P2Z receptors) and blocked by oxidized ATP, DIDS, suramin, amiloride, and KN62 (known inhibitors of

90 4-hydroxycinnamic acid (4 mM) or basolateral DIDS (1 mM) do not affect pHo regulation.

91 In planar lipid bilayers, DIDS inhibits ClC-ec1 activity reversibly, with an appar

92 application of the chloride channel blocker DIDS (100 microM) resulted in approximately 50% block of

93 or application of the Cl(-) channel blocker DIDS identifying it as a Ca(2+)-activated Cl(-) current

94 e dismutase (SOD), the anion channel blocker DIDS, and selective silencing of the chloride channel-3

95 was blocked by the anion transport blockers, DIDS and niflumic acid.

96 (A799G) exhibits reduced sensitivity to both DIDS and tenidap.

97 buffer, the slow phase was inhibited 70 % by DIDS.

98 itive to block by these divalent ions and by DIDS but the sensitivity of ClC-2 to block by cadmium io

99 lly induced depolarization was attenuated by DIDS (300 microM) and tamoxifen (1 microM), a response c

100 These currents were sensitive to block by DIDS, extracellular ATP and the antioestrogen compound t

101 (DIDS; 200 microM), although the blockade by DIDS was voltage dependent.

102 The current was blocked by DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic aci

103 larger at pH 6 than pH 8), and is blocked by DIDS in a voltage-dependent manner.

104 cellular Na(+) and HCO3(-) and is blocked by DIDS.

105 anion-conductive pathway that is blocked by DIDS.

106 mM Zn2+ or 10 microM Gd3+ but is blocked by DIDS.

107 s515 were the ATPase residues derivatized by DIDS.

108 id-induced epithelial injury was enhanced by DIDS and decreased by NPPB.

109 It was inhibited by DIDS (100 microM), Zn(2+) (100 microM), and by Gd(3+) (I

110 asolateral membrane Cl channels inhibited by DIDS and NPPB, respectively.

111 removal of HCO(3)(-)/CO(2) was inhibited by DIDS, acetazolamide, methazolamide, and low-chloride buf

112 This current is inhibited by DIDS, tamoxifen, IAA-94 and gadolinium.

113 ective currents, which were all inhibited by DIDS.

114 ed fraction of acid loading was inhibited by DIDS.

115 unaffected by glibenclamide but inhibited by DIDS.

116 tivity, reversibility, partial inhibition by DIDS and Mn2+) are shared with the flux pathway sometime

117 %) taurocholate transport from inhibition by DIDS in hepatocytes provides almost complete protection

118 monitored in conjunction with inhibition by DIDS.

119 Cross-linking of Lys492 and Lys515 by DIDS interfered with ATPase utilization of both ATP and

120 These deleterious effects were mediated by DIDS in a dose- and time-dependant manner, such that hig

121 S, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pharmacological properties o

122 aling" effects of O(2)(.-) were prevented by DIDS treatment, by depletion of intracellular Ca(2+) sto

123 e inhibited by NPPB or DPC and unaffected by DIDS.

124 At 23 degrees C, DIDS, an inhibitor of anion exchange, reduced basal 36Cl

125 (-) and initial presence of Na(+) and Cl(-), DIDS inhibited the changes in pH(i) produced by removal

126 (2) was inhibited by sodium-free conditions, DIDS, and the CA inhibitors acetazolamide and methazolam

127 The mutation Lys(539)Ala at the covalent DIDS-reaction site of AE1 reduced the DIDS sensitivity,

128 (115 mM) caused significant HCO3--dependent, DIDS-sensitive pHi recovery from intracellular acidosis,

129 in HEK cells resulted in a Na(+)-dependent, DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid)-

130 e effective blockers were voltage dependent; DIDS and NPPB were more effective at depolarized potenti

131 diisothiocyanato-stilbene-2, 2'-disulfonate (DIDS) in the WT but not in the mutant.

132 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) prevents both mitoNEET binding in vitro and mitoNE

133 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) reduces (DeltapH(S)*)(CO2) by half, but has no eff

134 -diisothiocyanato-stilbene-2,2'-disulfonate (DIDS) to inhibit all the HCO3-/Cl- transport protein (Ba

135 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS), 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPP

136 ,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), an inhibitor of band 3-mediated anion transport t

137 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS), and shRNA specific to the 1Na(+):2HCO(3)(-) cotra

138 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS), eliminates the remaining (DeltapH(S)*)(CO2) but h

139 '-diisothiocyanatostilbene-2,2'-disulfonate (DIDS; anion transport inhibitor), or with NBCe1-specific

140 4'-diisothiocyanostilbene-2,2'-disulphonate (DIDS) and 4,4'-dinitrostilbene-2,2'-disulphonate (SITS).

141 -diisothiocyanatostilbene-2,2'-disulphonate (DIDS), a blocker of Ca(2+)-activated Cl- channels, sugge

142 Recovery was unaffected by the stilbene drug DIDS (4,4-diisothiocyanatostilbene-disulphonic acid), bu

143 r this recording configuration an endogenous DIDS-sensitive Ca(2+)-activated Cl(-) conductance was al

144 on of niflumic acid and, to a lesser extent, DIDS to the hypotonic solution potentiated swelling and

145 conductance that was unaffected by external DIDS.

146 In the intact eye, DIDS and acetazolamide reduced AH secretion by 25% and 4

147 ovides almost complete protection (88%) from DIDS inhibition of hepatocyte cholate transport, suggest

148 em is almost completely protected (92%) from DIDS inhibition by this antibody in MDCK cells that expr

149 Furthermore, DIDS- modified membranes lack all low affinity ankyrin-b

150 +100 mV the order of potency was NFA > A9C > DIDS > DPC (K(i) (microm) = 10.1, 18.3, 48, and 111, res

151 and time-dependant manner, such that higher [DIDS] induced apoptosis more rapidly while apoptosis was

152 ded for 48 h, reduced cellular ATP; however, DIDS at 31 microM significantly reduced cellular ATP wit

153 d basal pH(i), whereas NPPB increased pH(i); DIDS further decreased pH(i) during acid challenge and a

154 n hallmarks of apoptosis were not present in DIDS treated cells, including mitochondrial fission and

155 nsitive to Cl- channel antagonists including DIDS (300 microM), tamoxifen (1 microM) and IAA-94 (100

156 al known Cl(-) channel inhibitors, including DIDS, tamoxifen, and 5-nitro-2-(3-phenylpropylamino)-ben

157 acetazolamide and the ion exchange inhibitor DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid

158 contrast, the Cl(-)-HCO3-exchange inhibitor DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic aci

159 y and increased sensitivity to the inhibitor DIDS.

160 he presence of the HCO3- transport inhibitor DIDS (4,4-di-isothiocyanatostilbene-2, 2-disulphonic aci

161 he presence of the anion transport inhibitor DIDS and the Cl(-) channel inhibitor, 5-nitro-2-(3-pheny

162 We used the anion transport inhibitor DIDS to investigate other members of the SLC26 family th

163 and blocked by the anion-transport inhibitor DIDS, and conclude that it is the renal electrogenic sod

164 susceptible to the anion transport inhibitor DIDS.

165 d by the addition of the exchange inhibitors DIDS (100 micromol/L) and ethylisopropylamiloride or by

166 In contrast, either 500 micromol/L DIDS, a concentration at which DIDS is known to act as a

167 pidly while apoptosis was observed at lower [DIDS] with prolonged exposure.

168 s reversed by mitoTEMPO, rotenone, malonate, DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid

169 The mean DIDS-inhibitable acid influx was equivalent in magnitude

170 ly 75% smaller in the presence of 200 microM DIDS, and absent in macropatches from H(2)O-injected ooc

171 nd 90% smaller in the presence of 200 microM DIDS.

172 be inhibited by niflumic acid (300 microM), DIDS (200 microM) and hypertonic solutions, and was virt

173 l- channel blockers NPPB (IC50 = 40 microM), DIDS (IC50 = 31 microM), tamoxifen (IC50 = 1.3 microM) a

174 ors, including: glibenclamide (100 microns), DIDS (100 and 500 microns), NPPB (100 microns) and Ba2+

175 oM) produced similar effects to NFA but 1 mM DIDS produced inhibition of I(Cl(Ca)) at both positive a

176 Prior addition of 1 mM DIDS to the NPE side decreased isoproterenol stimulation

177 microM forskolin) and were inhibited by 1 mM DIDS.

178 the currents were greatly attenuated by 1 mm DIDS.

179 naffected by NPPB but were inhibited by 3 mM DIDS in the basal bath.

180 HEPES substitution and addition of 0.5 mM DIDS reduced the acidification to 7-8% of control, respe

181 to 36% of control by the addition of 0.5 mM DIDS, a Na+/HCO3- cotransport blocker.

182 diphenylamine-2-carboxylic acid (DPC, 1 mM), DIDS (300 microM) and niflumic acid (100 microM).

183 he involvement of both NKCC1 and one or more DIDS-sensitive transporters in Cl(-) accumulation in olf

184 results suggest that NFA and DCDPC, but not DIDS, simultaneously enhance and block I(Cl(Ca)) by bind

185 ses AQP1 via the monomeric pore plus a novel DIDS-sensitive route that may be the central pore.

186 We have characterized the ability of DIDS and of selected N-hydroxysuccinimide cross-linking

187 (2+)], and at 35 degrees C in the absence of DIDS (when I(Cl(Ca)) is prominent), peak I(Cl(Ca)) also

188 potentially deleterious secondary effects of DIDS.

189 Serendipitously, the entry of DIDS-resistant HCMV also became independent of heparan s

190 Importantly, the data show that entry of DIDS-resistant virus became independent of heparan sulfa

191 in certain assays and future evaluations of DIDS as a neuroprotective agent should incorporate multi

192 oglycans (HSPGs), suggesting that evasion of DIDS lowered dependence on an initial interaction with H

193 To assess the impact of DIDS on cellular viability comprehensively we examined n

194 The side-dependent nature of DIDS inhibition will be useful for generating "functiona

195 eliminates the effects of pCMBS, but not of DIDS.

196 re was no increase in current on wash out of DIDS.

197 Although sequencing of DIDS-resistant HCMV revealed enrichment of a mutation wi

198 and analysis of pharmacological variants of DIDS suggested that intrinsic cysteine, and not lysine,

199 oduced with a molecular stoichiometry of one DIDS per ATPase.

200 e fully modified dimer does not bind DBDS or DIDS.

201 stores, or in the presence of either Gd3+ or DIDS.

202 on of alpha-IC function (bath CL- removal or DIDS, luminal bafilomycin) stimulated net HCO3- secretio

203 units capable of binding DBDS reversibly, or DIDS covalently, decreased nonlinearly in the absence of

204 ; both currents were prevented by suramin or DIDS pretreatment.

205 pal neurons occurs via NBCe1, and a parallel DIDS-sensitive, Cl- -dependent mechanism.

206 Together, pCMBS+DIDS reduce (DeltapH(S)*)(CO2) to zero.

207 ) and Cl(-) are transported through the same DIDS-sensitive channel(s).

208 in SMG acinar and duct cells showed separate DIDS-sensitive/EIPA-insensitive and DIDS-insensitive/EIP

209 of PE-side NaKCl cotransport and an NPE-side DIDS-inhibitable mechanism(s).

210 icated as the counterion efflux route, since DIDS inhibited the PGE2-stimulated cell volume change wi

211 nd basolateral side by NBCe1-specific siRNA, DIDS, or EIPA.

212 ic anion cotransport blockers, such as SITS, DIDS, furosemide, or bumetanide, when simultaneously add

213 ed as a 5,5'-diisothiocyanato-2-2'-stilbene (DIDS)-sensitive transporter in several tissues, while th

214 iisothiocyano-2,2'-disulfonic acid stilbene (DIDS) or niflumic acid (NFA).

215 iisothiocyano-2,2'-disulfonic acid stilbene (DIDS), and dextran sulfate (in a voltage-dependent manne

216 Cl- independent, and inhibited by stilbenes (DIDS and SITS).

217 The disulfonic stilbenes (DIDS and SITS) had markedly different effects and were f

218 We conclude that DIDS induces apoptosis in cultured hippocampal neurons,

219 Time-of-addition studies demonstrated that DIDS inhibited entry via direct interaction with the vir

220 ilities to both CO2 and HCO3-, we found that DIDS inhibited both Pm,HCO-3 and Pm,CO2, whereas intrace

221 We found that DIDS inhibits transporters specifically from the intrace

222 We found that DIDS reduced Pm,HCO-3 as expected, but also appeared to

223 in the H(+)-uncaging region, indicating that DIDS-sensitive transport is not an adequate pH-regulator

224 N-Terminal protein sequencing proved that DIDS treatment created AE2 homodimers.

225 As a proof of principle, we show that DIDS treatment inhibits repair of AID-initiated DNA brea

226 tivity with an anti-DIDS antibody shows that DIDS crosslinks hAQP1 monomers.

227 Results suggest that DIDS-sensitive, SCFA-dependent transport in the colonocy

228 in and electrical responses, suggesting that DIDS blocked the purinoceptor.

229 glycoprotein RL13, these did not explain the DIDS resistance phenotype.

230 Intriguingly, the DIDS-resistant virus demonstrated increased sensitivity

231 splice variants of NBC3 probably mediate the DIDS-insensitive/EIPA-sensitive NBC activity in the LM o

232 t indicated that pNBC1 probably mediates the DIDS-sensitive/EIPA-insensitive transport in the basolat

233 of the RL13 mutant partially phenocopied the DIDS resistance phenotype.

234 valent DIDS-reaction site of AE1 reduced the DIDS sensitivity, demonstrating that (1) the conductive

235 Similarly, the DIDS-insensitive influx was equivalent to that estimated

236 We find that the DIDS inhibitor does not alter the redox state of MitoNEE

237 s voltage-dependent than the blockade due to DIDS.

238 ers with their extracellular side exposed to DIDS function normally, maintaining stoichiometric proto

239 enum was similar to mannitol, insensitive to DIDS, and nonsaturable, indicating that it is predominan

240 tion by HOE and EIPA or the insensitivity to DIDS.

241 nt was sensitive to glibenclamide but not to DIDS, suggesting that a cystic fibrosis transmembrane co

242 Such currents were sensitive to DIDS (200-500 microm) and 5-nitro-2-(3-phenylpropylamino

243 exceeded that of mannitol, was sensitive to DIDS, and saturable, indicating transcellular secretion

244 g, acid retention at the core increased upon DIDS treatment, indicating that HCO3(-) ions are taken u

245 PC (diphenylamine-2-carboxylic acid) and was DIDS (4, 4'-diisothiocyanatostilbene-2,2'-disulfonic aci

246 blocker glibenclamide (250 microM), but was DIDS insensitive (500 microM).

247 Control cells were unchanged, whereas DIDS induced an apoptotic phenotype (chromatin condensat

248 iented in the bilayers, ascertaining whether DIDS inhibits from the intracellular or extracellular si

249 at 100 micromol/L, a concentration at which DIDS is an anion exchange inhibitor, minimally reduced n

250 00 micromol/L DIDS, a concentration at which DIDS is known to act as a Cl(-) channel blocker, or 10 m

251 The mechanism by which DIDS reduces CO2 permeability may not be through an acti

252 oriented" preparations of ClC-ec1, in which DIDS is used to silence transporters in one orientation

253 nce kinetic inhibitor replacement assay with DIDS (4,4'-diisothiocyanato-2,2'-stilbenedisulfonate) as

254 Cross-linking with DIDS implies a distance of approximately 13 A between Ly

255 in Pichia pastoris, treat spheroplasts with DIDS and examine hAQP1 by SDS-PAGE, reactivity with an a

256 Preincubation of dense SSRBCs with DIDS (4,4'-di-isothiocyanato-2,2'-disulfostilbene) inhib

257 Independent treatment with DIDS, at concentrations that had no effect on thymine di