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

8 DIDS has no effect on luminal alkalinization caused by t

9 DIDS is a commonly used anion channel antagonist that is

10 DIDS reduced baseline pH(i).

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

12 DIDS-inhibitable mechanisms, possibly including HCO3-Cl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Both acetazolamide and DIDS reduced chloride effluxes.

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

72 lonic NBC is sensitive to both amiloride and DIDS.

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

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

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

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

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

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

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

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

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

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

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

84 4-hydroxycinnamic acid (4 mM) or basolateral DIDS (1 mM) do not affect pHo regulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 anion-conductive pathway that is blocked by DIDS.

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

101 s515 were the ATPase residues derivatized by DIDS.

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

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

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

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

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

107 ective currents, which were all inhibited by DIDS.

108 ed fraction of acid loading was inhibited by DIDS.

109 unaffected by glibenclamide but inhibited by DIDS.

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

111 %) taurocholate transport from inhibition by DIDS in hepatocytes provides almost complete protection

112 monitored in conjunction with inhibition by DIDS.

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

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

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

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

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

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

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

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

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

122 (115 mM) caused significant HCO3--dependent, DIDS-sensitive pHi recovery from intracellular acidosis,

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

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

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

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

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

128 ,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), an inhibitor of band 3-mediated anion transport t

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

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

131 4'-diisothiocyanostilbene-2,2'-disulphonate (DIDS) and 4,4'-dinitrostilbene-2,2'-disulphonate (SITS).

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

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

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

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

136 conductance that was unaffected by external DIDS.

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

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

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

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

141 +100 mV the order of potency was NFA > A9C > DIDS > DPC (K(i) (microm) = 10.1, 18.3, 48, and 111, res

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

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

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

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

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

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

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

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

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

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

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

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

154 susceptible to the anion transport inhibitor DIDS.

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

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

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

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

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

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

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

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

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

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

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

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

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

168 the currents were greatly attenuated by 1 mm DIDS.

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

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

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

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

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

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

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

176 (2+)], and at 35 degrees C in the absence of DIDS (when I(Cl(Ca)) is prominent), peak I(Cl(Ca)) also

177 potentially deleterious secondary effects of DIDS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 We found that DIDS inhibits transporters specifically from the intrace

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 00 micromol/L DIDS, a concentration at which DIDS is known to act as a Cl(-) channel blocker, or 10 m

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

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

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

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

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

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