ライフサイエンスコーパス: Cl- channel

1 increases intraluminal liquidity by opening Cl channels.

2 nates in opening of a ciliary Ca2+-activated Cl- channel.

3 es, mediated by Kv1.3 and outward rectifying Cl- channels.

4 SLC26A7 and SLC26A9 function exclusively as Cl- channels.

5 iate the effects of presynaptic ligand-gated Cl- channels.

6 calcium-activated K+ channels, Na+,Ca2+, and Cl- channels.

7 and a subsequent opening of plasma membrane Cl- channels.

8 ) and pharmacologic inhibitors of epithelial Cl - channels.

9 ecting duct cells, claudin-4 functioned as a Cl(-) channel.

10 ICC express ANO1, a Ca(2+)-activated Cl(-) channel.

11 F transmembrane conductance regulator (CFTR) Cl(-) channel.

12 ithelium in which it probably functions as a Cl(-) channel.

13 fibrosis transmembrane conductance regulator Cl(-) channel.

14 s transmembrane conductance regulator (CFTR) Cl(-) channel.

15 al properties similar to the mammalian ClC-2 Cl(-) channel.

16 opens during the transport cycle to form the Cl(-) channel.

17 nductance regulator (CFTR), a cAMP-regulated Cl(-) channel.

18 chloride ion (Cl(-)) efflux through the CFTR Cl(-) channel.

19 nsmembrane glycoprotein and a cAMP-activated Cl(-) channel.

20 IP(3)R-dependent opening of Ca(2+)-activated Cl(-) channels.

21 s for eukaryotic Cl(-)/H(+) transporters and Cl(-) channels.

22 multiple cell types but did not affect CFTR Cl(-) channels.

23 defect mediated by the molecularly distinct Cl(-) channels.

24 consists of both Cl(-)/H(+) antiporters and Cl(-) channels.

25 is accomplished by Cl(-) efflux through ClC3 Cl(-) channels.

26 a(2+) channels in addition to functioning as Cl(-) channels.

27 s transmembrane conductance regulator (CFTR) Cl(-) channels.

28 macular dystrophy via dysfunction of hBest1 Cl(-) channels.

29 ayed deactivation of individual F508del-CFTR Cl(-) channels.

30 s transmembrane conductance regulator (CFTR) Cl(-) channels.

31 Bestrophins are a newly identified family of Cl(-) channels.

32 hrinkage by opening TMEM16A Ca(2+)-activated Cl(-) channels.

33 hibition of the cell surface density of CFTR Cl(-) channels.

34 function as both amino-acid transporters and Cl(-) channels.

35 cid (DIDS)-sensitive and gluconate-sensitive Cl(-) channels.

36 and also whether this protein functions as a Cl- channel, a Cl-/H+ antiporter, or as something else e

37 We find that antagonists of PLA(2) and Cl(-) channels abolish P2X7 receptor-mediated current fa

38 w external Ca(2+) solution chosen to prevent Cl(-) channel activation, suggesting OMP acts upstream o

39 activation, suggesting OMP acts upstream of Cl(-) channel activation.

40 ge through the additive effects of TRPV1 and Cl- channel activation.

41 A with ETX001 increased the Ca(2+)-activated Cl(-) channel activity and anion secretion in human bron

42 annel blocker CFTR(inh)-172 abolished apical Cl(-) channel activity in excised patches.

43 Moreover, apical Cl(-) channel activity was completely absent in principa

44 Low pH(o) activation of hClC-2 Cl(-) channel activity was PKA-dependent, retained in RG

45 Because DeltaF508-CFTR retains some Cl(-) channel activity, increased expression of DeltaF50

46 not a result of changes in cell viability or Cl(-) channel activity.

47 V mutation is associated with altered hBest1 Cl(-) channel activity.

48 tested the effect of RP-causing variants on Cl- channel activity and cellular localization of bestro

49 conductance regulator (CFTR) to inhibit its Cl- channel activity.

50 ded in this process is at least one K(+) and Cl(-) channel, allowing for both recycling of K(+) for t

51 GABA, an agonist of related Cl- channels, also triggered Cl- currents and secretion,

52 lytopic membrane protein that functions as a Cl(-) channel and consists of two membrane spanning doma

53 s transmembrane conductance regulator (CFTR) Cl(-) channel and contribute to fluid homeostasis in the

54 m single-molecule studies of an elasmobranch Cl(-) channel and later confirmed by crystal structures

55 changes in stomatal conductance of the slac1 Cl(-) channel and ost2 H(+)-ATPase mutants, which we ver

56 l conformation of the alpha1 glutamate-gated Cl(-) channel and the alpha1 glycine receptor.

57 The CLC protein fold is shared by Cl(-) channels and 2Cl(-):1H(+) antiporters.

58 1) and TMEM16B (ANO2), form Ca(2+)-activated Cl(-) channels and are important for transepithelial ion

59 two distinct mechanistic flavors: H(+)-gated Cl(-) channels and Cl(-)/H(+) antiporters.

60 The family of CLC proteins comprises both Cl(-) channels and Cl(-)/H(+) exchange transporters with

61 of Cl(-)-transporting proteins includes both Cl(-) channels and Cl(-)/H(+) exchange transporters.

62 The CLC protein family comprises both Cl(-) channels and H(+) -coupled anion transporters.

63 ay increase the cell surface density of CFTR Cl(-) channels and improve stability of pharmacologicall

64 channel (CLC) family comprises cell surface Cl(-) channels and intracellular Cl(-)/H(+) exchangers.

65 ngs to a family of putative Ca(2+)-activated Cl(-) channels and operates as membrane phospholipid scr

66 The TMEM16 family comprises Ca(2+)-activated Cl(-) channels and phospholipid scramblases.

67 terms of the hypotheses that bestrophins are Cl(-) channels and regulators of Ca signaling.

68 smic Cl(-) level is dynamically regulated by Cl(-) channels and transporters.

69 ipulation of epithelial ion (Na(+), K(+) and Cl(-)) channels and suppression of proinflammatory cytok

70 transduced signals through a Ca2+-activated Cl- channel and EGFR.

71 stic fibrosis transmembrane regulator (CFTR) Cl- channel and stimulation of ciliary beat frequency.

72 y phloretin, a blocker of swelling-activated Cl- channels and by flufenamic acid, a blocker of Cl- an

73 bited swelling-mediated activation of K+ and Cl- channels and cell volume recovery.

74 y, it has been proposed that bestrophins are Cl- channels and that the putative second transmembrane

75 family comprises H(+)-coupled exchangers and Cl(-) channels, and mutations causing their dysfunction

76 transmembrane ion fluxes via K(+) channels, Cl(-) channels, and voltage-operated Ca(2+) channels wer

77 (ICC-IM) by activation of Ca(2+) -activated Cl(-) channels (ANO1, encoded by Ano1) and voltage-depen

78 on, the latter by opening a Ca(2+)-activated Cl channel (ANO2) to elicit, unusually, an inward Cl cur

79 Here we show that the Ca(2+)-activated Cl ((-)) channel anoctamin-1 (ANO1/TMEM16A) is located i

80 The Ca(2+)-activated Cl(-) channel, anoctamin 1 (Ano1, also known as transmem

81 alpha(+) cells express the Ca(2+) -activated Cl(-) channel, anoctamin-1, across the entire renal pelv

82 current that was effectively blocked by the Cl(-) channel antagonist 5-nitro-2-(3-phenopropylamino)b

83 relative to controls; whereas apocynin, the Cl(-) channel antagonist 5-nitro-2-(3-phenylpropylamino)

84 The GlyR Cl(-) channel antagonist strychnine significantly blocke

85 ne was blocked by pretreatment with the GlyR Cl(-) channel antagonist strychnine.

86 )-facilitated NSCC in ICC was blocked by the Cl(-) channel antagonists 4,4'-diisothiocyanatostilbene-

87 h led us to question whether functional GlyR Cl(-) channels are expressed in ASM.

88 GlyR Cl(-) channels are expressed on ASM and regulate smooth

89 response to 8-Br-cAMP, indicating that CFTR Cl(-) channels are functional in embryonic kidneys and a

90 Because certain Cl(-) channels are proposed to promote apoptosis by redu

91 Bestrophin (BEST1-4) ligand-gated chloride (Cl(-)) channels are activated by calcium (Ca(2+)).

92 s transmembrane conductance regulator (CFTR) Cl(-) channel as a determinant in lysosomal acidificatio

93 strong possibility that the Ca(2+)-activated Cl(-) channels at the apical membrane are members of the

94 etory diarrheas increases the conductance of Cl(-) channels at the enterocyte luminal membrane, which

95 eatment of permeabilized myofibres with 2 mm Cl(-) channel blocker 9-anthracenecarboxylic acid (9AC)

96 titution of Cl(-) ions or application of the Cl(-) channel blocker DIDS identifying it as a Ca(2+)-ac

97 but unchanged by niflumic acid (100 mum), a Cl(-) channel blocker.

98 tro-2-(phenylpropylamino)-benzoate (NPPB), a Cl- channel blocker, reduced Isc stimulation by approxim

99 t was insensitive to apical disulphonic acid Cl(-) channel blockers, but sensitive to apical glibencl

100 well), which was reversibly inhibited by the Cl(-) channel blockers, phloretin (300 microM) or 5-nitr

101 opic taurine response was insensitive to the Cl(-) channel blockers, picrotoxin and strychnine, but i

102 )) influx that can be inhibited by selective Cl(-) channel blockers.

103 Addition of the Cl- channel blockers NPPB, glibenclamide, or bumetanide

104 The RVD was also inhibited by Cl--channel blockers and by Cl- substitution.

105 ity in a small subpopulation of F508del-CFTR Cl(-) channels but that the majority remain destabilized

106 C (100 microM) induced the openings of CFTR Cl channels by increasing its average open probability f

107 luable in the phenotypic studies of specific Cl- channels by limiting the effect of compensation on t

108 l conductance of endogenous Ca(2+)-dependent Cl- channels by lowering the energy barriers for ion tra

109 veral conductances, such as Ca(2+)-activated Cl() channels (CaCC) and non-selective cation channels (

110 ANO1 (TMEM16A) is a Ca(2+)-activated Cl(-) channel (CaCC) expressed in peripheral somatosenso

111 Activation of an apical Ca(2+)-dependent Cl(-) channel (CaCC) is the rate-limiting step for fluid

112 The newly discovered Ca(2+)-activated Cl(-) channel (CaCC), Anoctamin 1 (Ano1 or TMEM16A), has

113 pore-forming subunit of a Ca(2+) -dependent Cl(-) channel (CaCC), is activated by direct, voltage-de

114 The Ca(2+)-activated Cl(-) channel (CaCC), recently identified as TMEM16A, pl

115 er CaPLSase activity to the Ca(2+)-activated Cl(-) channel (CaCC).

116 was found recently to be a calcium-activated Cl(-) channel (CaCC).

117 dent kinase II (CaMKII) and Ca(2+)-activated Cl(-) channels (CaCC) because simultaneous addition of m

118 el, and (b) secretion, by the Ca2+-activated Cl- channel (CaCC) and CFTR.

119 uctance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC).

120 An antagonist of calcium-sensitive Cl- channels (CaCC), niflumic acid, had little effect on

121 Ca(2+)-activated Cl(-) channels (CaCCs) are exceptionally well adapted to

122 Ca(2+)-activated Cl(-) channels (CaCCs) are key regulators of numerous ph

123 physiological importance of Ca(2+)-activated Cl(-) channels (CaCCs) in neurons has been largely overl

124 ily that includes TMEM16A/B Ca(2+)-activated Cl(-) channels (CaCCs) is linked to Scott syndrome with

125 t has been postulated that calcium-activated Cl(-) channels (CaCCs) play a role in airway epithelial

126 ian TMEM16A and TMEM16B are Ca(2+)-activated Cl(-) channels (CaCCs), whereas mammalian TMEM16F, funga

127 ustained by the activity of Ca(2+)-activated Cl(-) channels (CaCCs).

128 ctance regulator (CFTR) and Ca(2+)-activated Cl(-) channels (CaCCs).

129 n may occur via activation of Ca2+-activated Cl- channels (CaCCs) or an increase in the Cl- driving f

130 Ca(2+)-activated Cl- channels (CaCCs) perform many important functions in

131 have deleterious mutations in an epithelial Cl(-) channel called the CF transmembrane conductance re

132 channel in turn activates a Ca(2+)-activated Cl(-) channel, causing a Cl(-) efflux and further depola

133 s transmembrane conductance regulator (CFTR) Cl(-) channel, causing airway surface liquid dehydration

134 fibrosis transmembrane conductance regulator Cl- channel (CFTR) participates in phagosomal pH control

135 Although commonly known as a Cl(-) channel, CFTR also conducts thiocyanate (SCN(-)) i

136 K(+) channel Kir4.1, and stimulation of the Cl(-) channel ClC-K.

137 The voltage-gated Cl(-) channel (CLC) family comprises cell surface Cl(-)

138 The Ca2+-activated Cl- channel (CLCA) inhibitor, niflumic acid (NFA, 100 mi

139 here we demonstrate that the C. elegans ClC Cl(-) channel CLH-1 is highly permeable to HCO3 (-) and

140 on was initiated by Cl - secretion via ClC-2 Cl - channels co-expressed with occludin and localized t

141 cal component of the acinar Ca(2+)-activated Cl(-) channel complex that is essential for saliva produ

142 to insulin is mediated through exocytosis of Cl- channel-containing vesicles and a subsequent opening

143 pore region of the TMEM16A Ca(2+)-activated Cl(-) channel convert it into a robust scramblase.

144 nward-rectifying K+ channels and background (Cl- channel) current, and to a parallel loss in sensitiv

145 The cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance

146 ful approach to understanding the epithelial Cl(-) channel cystic fibrosis transmembrane conductance

147 conductance regulator (CFTR) is an ATP-gated Cl(-) channel defective in the genetic disease cystic fi

148 linity, we used mutants of the only vacuolar Cl(-) channel described to date: the Arabidopsis (Arabid

149 ast, picrotoxin, which blocks the GABA-gated Cl- channel, did not inhibit the secondary rise in [Cl-]

150 transmembrane conductance regulator (CFTR, a Cl(-) channel) disrupt salt and fluid transport and lead

151 eutral ion channel, and of GlyR, an inactive Cl(-) channel, do not cause CFAs, demonstrating that cor

152 the first observation of the involvement of Cl(-) channels during the HCV life cycle.

153 -) ion channels, it is controversial whether Cl(-) channel dysfunction can explain the diseases.

154 l myocytes, suppression of Ca(2+) -activated Cl(-) channels eliminated AP duration alternans, but pro

155 (ICC-IM) by activation of Ca(2+) -activated Cl(-) channels (encoded by Ano1) and voltage-dependent L

156 (including ICC-IM) express Ca(2+) -activated Cl(-) channels, encoded by Ano1, and rely upon this cond

157 Previously, we provided evidence that single Cl-channel events underlie DAT-1 currents.

158 3',5'-cyclic monophosphate (cAMP)-stimulated Cl(-) channel expressed in cholangiocytes.

159 uctance regulator (CFTR) is a cAMP-activated Cl(-) channel expressed in the apical membrane of fluid-

160 uctance regulator (CFTR) is a cAMP-activated Cl(-) channel expressed in the apical plasma membrane of

161 brane conductance regulator (CFTR) chloride (Cl(-)) channel expression and fluid secretion in the air

162 PAC suggests a broad role for this conserved Cl(-) channel family in physiological and pathological p

163 The CLC 'Cl(-) channel' family consists of both Cl(-)/H(+) antipo

164 om two distinct families of Ca(2+)-activated Cl(-) channels found in salivary glands.

165 lation of the function of ClC-0, a chloride (Cl(-)) channel from the Torpedo electric organ.

166 Regulation of the CFTR Cl channel function involves a protein complex of activa

167 Q1291F CFTR displayed significantly reduced Cl(-) channel function in well differentiated primary hu

168 ns of adenosine 5'-monophosphate (AMP), CFTR Cl(-) channel function is coupled to adenylate kinase ac

169 rmine whether the A243V mutation affects the Cl(-) channel function of hBest1.

170 rophy (BVMD) is caused by dysfunction in the Cl(-) channel function of human bestrophin-1 (hBest1), b

171 re reported to alter Na(+), K(+), Ca(2+) and Cl(-) channel function, intracellular [Ca(2+)], and Na(+

172 A243V mutations does not correlate with the Cl(-) channel function, the results also support the sug

173 26a9 has both nCl(-)-HCO(3)(-) exchanger and Cl(-) channel function.

174 the effect of the hBest1 mutation on hBest1 Cl(-) channel function.

175 except L567F and T216I produced a defect in Cl(-) channel function.

176 suggesting that this mutation may not affect Cl(-) channel function.

177 erated AFC in this model is due to increased Cl- channel function.

178 a Ca(2+) influx that opens Ca(2+)-activated Cl(-) channels, generating the receptor potential.

179 nt studies have identified several chloride (Cl-) channel genes in the heart, including CFTR, ClC-2,

180 A modified invertebrate glutamate-gated Cl(-) channel (GluCl alphabeta) was previously employed

181 cently a novel cGMP-activated Ca2+-dependent Cl- channel has been described in rat mesenteric artery

182 e large superfamily of ClC voltage-dependent Cl(-) channels, has been proposed as a molecular candida

183 Until recently, anion (Cl(-)) channels have received considerably less attentio

184 iously prime candidates for Ca(2+)-activated Cl(-) channels, have been supplanted by the newly discov

185 or pathophysiological phenotypes of cardiac Cl- channels, however, may be complicated by the compens

186 functions as a Cl(-)/H(+) antiporter, not a Cl(-) channel; however, the molecular mechanism for Cl(-

187 fibrosis transmembrane conductance regulator Cl(-) channel; however, the relative alignment of these

188 ibrosis transmembrane conductance regulator, Cl(-) channel in BECs and suggest that TMEM16A may be a

189 n apical cell membranes or its function as a Cl(-) channel in native renal epithelia has not been dem

190 ods, Eriksen et al. (2016) have identified a Cl(-) channel in the transporter that is coactivated by

191 tically subjective essay recalls the Torpedo Cl(-) channel in the years when it had neither a molecul

192 experiments revealed expression of GABA(A)R Cl(-) channels in 52% of beta-cells (current density 9 p

193 s transmembrane conductance regulator (CFTR) Cl(-) channels in mammalian cells revealed confined diff

194 Cl(-) channels in the apical membrane of biliary epithel

195 CFTR forms protein kinase A (PKA)-activated Cl(-) channels in the apical membrane of principal cells

196 the local apical Ca2+ spikes that switch on Cl(-) channels in the apical plasma membrane as well as

197 c reticulum and leads to the absence of CFTR Cl(-) channels in the apical plasma membrane.

198 ogenesis, but little is known about roles of Cl(-) channels in the associated processes.

199 We summarise what is known regarding Cl(-) channels in the ER/SR and the non-selective cation

200 d, in part, by modulating the number of CFTR Cl(-) channels in the plasma membrane by adjusting CFTR

201 TMEM16A), also termed Anoctamin 1, chloride (Cl(-)) channels in arterial myocytes.

202 solute carrier family 26, member 9 (SLC26A9) Cl- channel in asthma, we induced Th2-mediated inflammat

203 g of the integrated function of each cardiac Cl- channel in the context of health and disease.

204 to delineate the functional role of cardiac Cl- channels in the context of health and disease.

205 We summarise what is known regarding Cl- channels in the ER/SR and the non-selective cation c

206 ted (CNG) channel, leading to Ca2+ gating of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2+ -activated Cl

207 mulates cAMP production to activate the CFTR Cl(-) channel, increase ciliary beating, and initiate cy

208 Natural-product diarrhea remedies with Cl(-) channel inhibition activity have also been identif

209 apid, protein kinase C (PKC)-dependent ClC-1 Cl(-) channel inhibition in rodent muscle.

210 RNA)-mediated silencing, we demonstrate that Cl(-) channel inhibition is detrimental to HCV replicati

211 Exposure to a Cl(-) channel inhibitor 5-nitro-2-(3-phenylpropylamino)b

212 ree" solution and blocked by the nonspecific Cl(-) channel inhibitor niflumic acid and by preincubati

213 trans-membrane conductance regulator (CFTR) Cl(-) channel is a multimer.

214 Bestrophin-2 (Best2), a putative Cl(-) channel is expressed in the nonpigmented epitheliu

215 molecular identity of this Ca(2+)-activated Cl(-) channel is unknown.

216 Although activation of outward rectifying Cl(-) channels is one of the fastest responses of endoth

217 Our data demonstrate that the SLC26A9 Cl- channel is activated in airway inflammation and sugg

218 Knowledge of how ATP gates the CFTR Cl- channel is critical for understanding CFTR's physiol

219 It is not known whether the activity of Cl- channels is altered in insulin resistance and by whi

220 that electrolyte and fluid efflux via K+ and Cl- channels is controlled by swelling-induced activatio

221 Ano1 (Tmem16a), a Ca(2+)-activated Cl(-) channel, is an ion channel expressed in ICC.

222 amongst other factors, the expression of the Cl channel kidney-specific chloride channel 1 and its su

223 ClC Cl- channels make up a large molecular family, ubiquitou

224 s transmembrane conductance regulator (CFTR) Cl(-) channel may be of value in developing new treatmen

225 ructurally unrelated prosecretory intestinal Cl(-) channels may account for its intestinal antisecret

226 It has been shown that Cl- channels may contribute to cardiac arrhythmogenesis,

227 The integrated function of Cl- channels may involve multi-protein complexes of the

228 uman macrophages and suggest that PLA(2) and Cl(-) channels mediate innate immunity downstream of P2X

229 ermined in the intestine, this voltage-gated Cl(-) channel might compensate for the secretory defects

230 16A) and ANO2 (TMEM16B) are Ca(2+)-activated Cl(-) channels, most ANO paralogs are Ca(2+)-dependent p

231 s transmembrane conductance regulator (CFTR) Cl(-) channel mutations cause cystic fibrosis lung disea

232 y reflect upregulation of swelling-activated Cl(-) channels of different subtypes, especially when th

233 sed by defects in the CFTR, a cAMP-activated Cl- channel of epithelia.

234 regulates inward-rectifying K+ channels and Cl- channels of Vicia guard cells via intracellular Ca2+

235 aying, in part via the LGC-55 tyramine-gated Cl(-) channel on the HSNs.

236 ss the physiologic implications of open CFTR Cl(-) channels on salt handling by the collecting duct a

237 ation by Na(+)-coupled uptake, glycine opens Cl(-) channels on the surface membrane.

238 ed the effects of fatty acid accumulation on Cl- channel opening in a model liver cell line.

239 ion of PKC partially restored exocytosis and Cl- channel opening in insulin-resistant cells.

240 r, insulin failed to activate exocytosis and Cl- channel opening.

241 sporters form dimers that function either as Cl(-) channels or as electrogenic Cl(-)/H(+) exchangers.

242 The maxi Cl- channel (p-VDAC) blocker Gd3+, the ClC-2 inhibitor C

243 e that hClCa1 does not form Ca(2+)-dependent Cl- channels per se or enhance the trafficking/insertion

244 One reason for this may be that many Cl(-) channels perform functions that might be considere

245 ad no effect, suggesting that flow-activated Cl(-) channels play an important role in regulating EC f

246 s transmembrane conductance regulator (CFTR) Cl- channel plays vital roles in fluid transport in many

247 BEST1 is a Ca(2+)-activated Cl(-) channel predominantly expressed in retinal pigment

248 Inhibition of Ca(2+) -activated Cl(-) channels reduced beat-to-beat AP alternations, but

249 ine CFTR formed a weakly inwardly rectifying Cl(-) channel regulated by PKA-dependent phosphorylation

250 Enterocyte Cl(-) channels represent an attractive class of targets

251 fibrosis transmembrane conductance regulator Cl(-) channel requires a functionally unique, positively

252 the plasma membrane, and it blocked K(+) and Cl(-) channel responses to abscisic acid in guard cells.

253 is thought to function as a Ca(2+)-activated Cl(-) channel, RPE cells from Best1(W93C) mice exhibited

254 We set out to identify Cl(-) channel(s) and/or transporter(s) that are regulate

255 channels (VDCCs) or TMEM16A Ca(2+)-activated Cl(-) channels significantly changes global cytosolic Ca

256 s may involve multi-protein complexes of the Cl- channel subproteome and similar phenotypes can be at

257 Our results identify the first Cl(-) channel target of the CLCA family of proteins and

258 Bestrophin is thought to be the Cl channel that generates the LP.

259 nductance regulator (CFTR), a cAMP-dependent Cl channel that regulates epithelial surface fluid secre

260 ligand-gated ion channels, is an inhibitory Cl(-) channel that is gated by glycine.

261 gs reveal that SLC26A7 functions as a unique Cl(-) channel that is regulated by intracellular H(+).

262 ANO1 (TMEM16A) is a Ca(2+)-activated Cl(-) channel that regulates diverse cellular functions

263 rst described as a family of plasma membrane Cl(-) channels that could be activated by calcium.

264 The cftr gene codes for a Cl(-) channel, the cystic fibrosis transmembrane conduct

265 Chloride influx through GABA-gated Cl(-) channels, the principal mechanism for inhibiting n

266 ace in mice through Ca2+- and cAMP-sensitive Cl- channels, the latter pathway being the cystic fibros

267 quence of an activation of [Ca2+]c sensitive Cl- channels, the model simulations compare well with th

268 mediated by activation of Ca(2+) -activated Cl(-) channels; thus, Ca(2+) signalling is central to th

269 gly inhibit the intestinal calcium-activated Cl(-) channel TMEM16A by a voltage-independent inhibitio

270 d the protein levels of the Ca(2+)-activated Cl(-) channel TMEM16A, the major apical Cl(-) efflux pat

271 family, which includes the Ca(2+)-activated Cl(-) channels TMEM16A and TMEM16B and a small-conductan

272 hy with subcortical cysts, targets the CLC-2 Cl(-) channel to cell contacts in glia and activates CLC

273 rks can additionally activate Ca2+-activated Cl(-) channels to generate spontaneous transient inward

274 CaMKII) activation of ClC-3, a voltage-gated Cl(-) channel/transporter, because pharmacological inhib

275 validated the idea that ions permeate TMEM16 Cl(-) channels via a structurally homologous pathway by

276 tructural components of the volume-regulated Cl(-) channel (VRAC), and we underline the intriguing po

277 ial of the inward current, indicating that a Cl- channel was not involved.

278 The expression of candidate Cl- channels was confirmed by RT-PCR.

279 n agonist of glycine receptor chloride (GlyR Cl(-)) channels, was found to relax contracted ASM, whic

280 To study individual CFTR Cl(-) channels, we performed single-channel recording, w

281 Ca2+ -activated Cl channels were recently discovered to be encoded by me

282 The 2 mutant Cl(-) channels were equally slow to open, suggesting tha

283 These Cl(-) channels were observed in cell-attached apical pat

284 Quiescent Cl(-) channels were present in patches excised from untr

285 ce, kinetics, and anion selectivity of these Cl(-) channels were the same as those of recombinant mou

286 elopment of agents that act directly to open Cl channels, which thereby increases the liquidity of th

287 stic fibrosis transmembrane regulator (CFTR) Cl(-) channel, which is regulated by phosphorylation in

288 trimerization domains is a partially formed Cl(-) channel, which opens to form a pore through which

289 e Ca(2+) activates Ca(2+)-dependent K(+) and Cl(-) channels, which participate in bleb regulation.

290 conductance regulator (CFTR) is a chloride (Cl(-)) channel, which plays an important role in physiol

291 mily of calcium (Ca(2+))-activated chloride (Cl(-)) channels, which mediate the influx and efflux of

292 Single Ca(2+)-activated Cl() channels with a unitary conductance of 7.8 pS were

293 e conclude that ovine CFTR forms a regulated Cl(-) channel with enhanced conductance and ATP-dependen

294 stic fibrosis transmembrane regulator (CFTR) Cl(-) channel with maximum inhibition of approximately 6

295 we report that SLC26A9 is a highly selective Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability

296 These findings indicate that SLC26A9 is a Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability.

297 cells SLC26A7 functions as a pH(i)-regulated Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability.

298 M16A) is a widely expressed Ca(2+)-activated Cl(-) channel with various physiological functions rangi

299 discuss the recent explosion of interest in Cl(-) channels, with special emphasis on new and often s

300 amins and now hold a tenuous position in the Cl(-) channel world.