ライフサイエンスコーパス: anion channel

1 o those produced by activation of the LGC-55 anion channel.

2 tive SLAH2 into a chloride/nitrate-permeable anion channel.

3 nnel 1 (SLAC1) homolog 3] and activated this anion channel.

4 ance regulator (CFTR) gene, which encodes an anion channel.

5 subunits contribute to form the pore of this anion channel.

6 fibrosis transmembrane conductance regulator anion channel.

7 s transmembrane conductance regulator (CFTR) anion channel.

8 activation of a ROS-sensitive inner membrane anion channel.

9 tical for survival such as voltage-dependent anion channel.

10 8 affect the expression of voltage-dependent anion channel.

11 hat functions as a phosphorylation-regulated anion channel.

12 ther glia, and it serves dual function as an anion channel.

13 s transmembrane conductance regulator (CFTR) anion channel.

14 s transmembrane conductance regulator (CFTR) anion channel.

15 the gating mechanisms of the EAAT-associated anion channel.

16 nducting) converted into chloride-conducting anion channels.

17 the first identified auxiliary subunits for anion channels.

18 gle-channel current amplitudes of associated anion channels.

19 exhibited the hallmark properties of S-type anion channels.

20 ertebrates, not affecting human ligand-gated anion channels.

21 glutamate transporters but also function as anion channels.

22 scle cells (PASMCs), but little is known for anion channels.

23 stomatal closing and HCO(3)(-) activation of anion channels.

24 ulfonic acid, a blocker for volume-activated anion channels.

25 genic Cl-/HCO(3)- exchangers or as bona fide anion channels.

26 glutamate transporters and volume-activated anion channels.

27 2L1, VMD2L2, and VMD2L3) are a new family of anion channels.

28 ition to advances in the design of synthetic anion channels.

29 red bicarbonate-induced activation of S-type anion channels.

30 ects in epithelia, close to those of natural anion channels.

31 t of the response that is likely mediated by anion channels.

32 (iii) Voltage-dependent anion channel 1 (a mitochondrial and plasma membrane pro

33 xpression, CPK21 interacted with SLAH3 [slow anion channel 1 (SLAC1) homolog 3] and activated this an

34 The voltage-dependent anion channel 1 (VDAC-1) is an important protein of the

35 ndrial calcium released by voltage-dependent anion channel 1 (VDAC1) after sciatic nerve injury trigg

36 ed proteins, in particular voltage-dependent anion channel 1 (VDAC1) and contactin-associated protein

37 receptors (IP3Rs) and the voltage-dependent anion channel 1 (VDAC1) at the outer mitochondrial membr

38 inducer, overexpression of voltage-dependent anion channel 1 (VDAC1) induced Parkin translocation to

39 chondrial membrane protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a var

40 lycine directly bounded to voltage dependent anion channel 1 (VDAC1) on the mitochondrial outer membr

41 ylated StAR interacts with voltage-dependent anion channel 1 (VDAC1) on the OMM, which then facilitat

42 nalysis, the expression of voltage-dependent anion channel 1 (VDAC1), a constituent of the mitochondr

43 The voltage-dependent anion channel 1 (VDAC1), found in the mitochondrial oute

44 abolism and apoptosis, the voltage-dependent anion channel 1 (VDAC1), was linked to chemoresistance w

45 e the relationship between voltage-dependent anion channel 1 protein (VDAC1) and amyloid beta (Abeta)

46 lex composed of the VDAC1 (voltage-dependent anion channel 1), the GRP75 (chaperone glucose-regulated

47 eracting proteins were the voltage-dependent anion channels 1, 2, and 3 (VDACs 1, 2, and 3), pore-for

48 d ligand in the IMP, mouse voltage-dependent anion channel-1 (mVDAC1), and top-down MS confirmed a si

49 Voltage-dependent anion channel-1 (VDAC1) is a highly regulated beta-barre

50 Human mitochondrial voltage-dependent anion channel 2 (hVDAC-2), the most predominant isoform

51 er the mitochondrial porin voltage-dependent anion channel 2 (VDAC2) as essential component and platf

52 e that StAR interacts with voltage-dependent anion channel 2 (VDAC2) at the mitochondria-associated e

53 Human voltage-dependent anion channel-2 (hVDAC-2) functions primarily as the cru

54 TPR3 binds to voltage-dependent anion channel 3, but although this is sufficient for cen

55 genes responsible for the plasmodial surface anion channel, a nutrient channel that also transports i

56 yers, LRRC8 complexes are sufficient to form anion channels activated by osmolality gradients.

57 SLAH3/CPK21 protein complex, and as a result anion channel activation failed.

58 ts cytosolic Ca(2+) signaling and downstream anion channel activation in a PAD4-dependent manner.

59 e intracellular Ca(2+) sensitivity of S-type anion channel activation in wild-type and ht1-2 kinase m

60 ate flux were isolated and measured, and the anion channel activation was fitted to analytical expres

61 d enhanced bicarbonate sensitivity of S-type anion channel activation.

62 Whereas anion channel activity has been extensively investigated

63 of its maturation, trafficking and regulated anion channel activity in human airway epithelial cells.

64 DeltaR) and found that it retained regulated anion channel activity in vitro.

65 Anion channel activity is known to depend on phosphoryla

66 s to the C-terminus resulted in constitutive anion channel activity.

67 ility transition pore (ie, voltage-dependent anion channel, adenine nucleotide translocase, cyclophil

68 ty, such as cyclophilin D, voltage-dependent anion channel, adenine nucleotide transporter, and ATP s

69 ic calcium (Ca(2+)) activates the bestrophin anion channel, allowing chloride ions to flow down their

70 onductance regulator (CFTR) is an epithelial anion channel and a key regulator of electrolyte and flu

71 ssible association between voltage-dependent anion channel and glucose-regulated protein 78 on the su

72 es binding to cell surface voltage-dependent anion channel and is inhibited by human hexokinase I.

73 er, kringle 5 acts through voltage-dependent anion channel and microplasminogen does so via the gluco

74 is essential for the activation of the SLAC1 anion channel and stomatal closing.

75 ria, whereas levels of the voltage-dependent anion channel and the adenine nucleotide translocase wer

76 ns, including the abundant voltage-dependent anion channel and the cation-preferring protein-conducti

77 Both the voltage-dependent anion channel and the glucose-regulated protein 78 have

78 ted SLAC1 into a SLAH2-like nitrate-specific anion channel and vice versa.

79 had more O-GlcNAc-modified voltage-dependent anion channel and were more resistant to calcium-induced

80 Anion channels and antiporters of the ClC superfamily ha

81 We characterized anion channels and CPK transcripts in PTs and analyzed t

82 ability of cytosolic Ca2+ to activate S-type anion channels and down-regulate inward-rectifying K+ ch

83 s appear, including with the plasma membrane anion channels and H(+)-ATPase and with the tonoplast TP

84 s transmembrane conductance regulator (CFTR) anion channels and solute carrier family 26 member A6 (S

85 Eukaryotic CLC anion channels and transporters are homodimeric proteins

86 ClC-3 is a member of the CLC family of anion channels and transporters, for which multiple func

87 ty that ClC-7, a member of the CLC family of anion channels and transporters, is a contributor to thi

88 ist, no other type of neurotransmitter-gated anion channel, and thus no other source of fast synaptic

89 ial complex I, complex II, voltage-dependent anion channels, and benzodiazepine receptor, respectivel

90 glutamate transporters but also function as anion channels, and different EAATs vary considerably in

91 DIDS is a commonly used anion channel antagonist that is putatively cytoprotecti

92 Moreover, the voltage-dependent anion channel antagonist TRO19622 had no effect on ATP r

93 th superoxide dismutase (SOD), (2) a general anion channel antagonist, or (3) the Nox inhibitor apocy

94 CLC anion channels are homodimeric proteins.

95 The signaling mechanisms that regulate CLC anion channels are poorly understood.

96 teomic analysis identified voltage-dependent anion channel as a potential target of O-GlcNAc modifica

97 ted protein 25, as well as voltage-dependent anion channels as potential facilitators of the general

98 lation of H2 O2 and NO, upregulation of SLOW ANION CHANNEL ASSOCIATED 1 (SLAC1) gene expression and r

99 ightly less effective than CFTR, the natural anion channel associated with CF.

100 t protein (YFP) tagging of a homolog of SLOW ANION CHANNEL-ASSOCIATED1 (SLAH3:YFP) was widespread alo

101 ion of iChS by chemical modifications favors anion channeling at the expense of substrate transport,

102 s in regulating the activity of the vacuolar anion channel AtALMT9.

103 Metal-organic anion channels based on Zn10 L15 pentagonal prisms have

104 ansporter 1 (Nkcc1) and the Ca(2+)-activated anion channel Bestrophin 2 (Best2), as well as glycoprot

105 tion with either superoxide dismutase or the anion channel blocker 4'-diisothiocyanostilbene-2,2'-dis

106 ), ABCB19, increases upon treatment with the anion channel blocker 5-nitro-2-(3-phenylpropylamino)-be

107 inhibited by superoxide dismutase (SOD), the anion channel blocker DIDS, and selective silencing of t

108 ent, inhibition of ATP release with the maxi-anion channel blocker gadolinium chloride, or siRNA sile

109 as inhibited by treatment with either of two anion channel blockers, 4'-diisothiocyano-2,2'-disulfoni

110 nnels and to activate current carried by the anion channels, both of which are sensitive to [Ca(2+)]i

111 hat HT1 inhibits the activation of the SLAC1 anion channel by the protein kinases OPEN STOMATA1 and G

112 e bicarbonate permeability (P HC O3/ Cl ) of anion channels by reducing energy barriers of size-exclu

113 e that leads to the activation of guard cell anion channels by the protein kinase OPEN STOMATA1.

114 rane conductance regulator (CFTR) epithelial anion channel cause cystic fibrosis (CF).

115 s transmembrane conductance regulator (CFTR) anion channel causes misfolding and premature degradatio

116 (ROS)-induced opening of the inner membrane anion channel causes transient mitochondrial depolarizat

117 the oligomerization of the voltage-dependent anion channels causing a shift of calcium from the ER to

118 3',5'-cyclic monophosphate (cAMP)-activated anion channel CFTR mediates Cl(-)-dependent fluid secret

119 Inhibitors of NADPH oxidase and anion channel ClC3 blocked TNF-induced VCAM expression,

120 smembrane conductance regulator (CFTR) is an anion channel composed of 1480 amino acids.

121 The plant SLAC1 anion channel controls turgor pressure in the aperture-d

122 4) in Xenopus laevis oocytes elicited S-type anion channel currents.

123 ed by mutations in the gene encoding for the anion channel cystic fibrosis transmembrane conductance

124 ) is caused by dysfunction of the epithelial anion channel cystic fibrosis transmembrane conductance

125 ived from the plasma membrane, including the anion channel cystic fibrosis transmembrane conductance

126 ucidate a novel mechanism placing cation and anion channels downstream of ligand-mediated [Ca(2+)](i)

127 g events that result in activation of S-type anion channels during stomatal closure, providing a spec

128 a of the dual-function glutamate transporter/anion channel EAAT1, and discovered it caused malformati

129 smembrane conductance regulator (CFTR) is an anion channel evolved from an ATP-binding cassette trans

130 smembrane conductance regulator (CFTR) is an anion channel evolved from the ATP-binding cassette (ABC

131 of mitochondria (porin, a voltage-dependent anion channel expressed on all mitochondria) and axons (

132 d epithelial mitochondrial voltage-dependent anion channel expression were observed 3 days after DSS.

133 ansmembrane conductance regulator (CFTR), an anion channel found mainly in apical membranes of epithe

134 rent beta-barrel channels: voltage-dependent anion channel from outer mitochondrial membrane VDAC, ba

135 l rhodopsins (ACRs), a family of light-gated anion channels from cryptophyte algae that provide highl

136 s transmembrane conductance regulator (CFTR) anion channel function causes cystic fibrosis (CF) lung

137 cle and that these effects result in changed anion channel function.

138 opus laevis oocytes, and their transport and anion channel functions were investigated.

139 An expression pattern analysis of ACh-gated anion channels furthermore suggests that ACh may also op

140 Twelve subunits are predicted to form anion channels gated by gamma-aminobutyric acid (GABA),

141 The QUAC1/ALMT12 anion channel heterologous expressed in oocytes was gate

142 zed the Caenorhabditis elegans CLC-1/2/Ka/Kb anion channel homolog CLH-3b to characterize the regulat

143 In guard cells, activation of anion channels (I(anion)) is an early event leading to s

144 cated in the activation of an inner membrane anion channel (IMAC), distinct from the permeability tra

145 transition pore (mPTP) or the inner membrane anion channel (IMAC), respectively.

146 g ROS-sensitive mitochondrial inner membrane anion channels (IMAC), and slow depolarization waves rel

147 asome via inhibition of the volume-regulated anion channel in macrophages, independently of COX enzym

148 smembrane conductance regulator (CFTR) is an anion channel in the ATP-binding cassette (ABC) transpor

149 veloped a Markov model of the inner membrane anion channel in which reactive-oxidative-species (ROS)-

150 they might replace the activity of defective anion channels in conditions such as cystic fibrosis.

151 indicating that these 2 MPKs act upstream of anion channels in guard cell ABA signaling.

152 thermore, ABA and calcium failed to activate anion channels in guard cells of mpk9-1/12-1, indicating

153 tions as a small-molecule activator of SLAC1 anion channels in guard cells.

154 ly, several studies have indicated a role of anion channels in NLRP3 inflammasome assembly, but their

155 malate transporters (ALMTs) form a family of anion channels in plants, but little is known about most

156 ion and the molecular constituents of native anion channels in vivo.

157 I as a specific ligand for voltage-dependent anion channel, in addition to kringle 5.

158 inly responsible for fluid absorption, while anion channels, including CFTR and Ca(2+)-activated chlo

159 CFTR is an anion channel involved in fluid secretion and mutated in

160 protein kinase A (PKA)-activated epithelial anion channel involved in salt and fluid transport in mu

161 sporters (ALMTs) form an important family of anion channels involved in fundamental physiological pro

162 rane conductance regulator (CFTR) epithelial anion channel is a large multidomain membrane protein th

163 The CFTR anion channel is controlled by ATP binding and enzymatic

164 The mutated CFTR anion channel is not fully glycosylated and shows minima

165 (GlyR), revealed that the ion selectivity of anion channels is basically determined by the electric p

166 The selectivity filter of SLAC/SLAH anion channels is determined by the polarity of pore-lin

167 intracellular modulators of the activity of anion channels is fundamental to understanding their phy

168 wever, the mechanism of ion selection by the anion channels is largely unknown.

169 Gating of EAAT anion channels is tightly coupled to transitions within

170 hat the OST1 kinase interacts with the SLAC1 anion channel, leading to its activation via phosphoryla

171 arylethynyl strands and resembles a tubular anion channel lined with nine halogen bond donors.

172 nd cyclophilin D (possibly voltage-dependent anion channel), may be the functional downstream target(

173 The regulation of the anion channels of the ALMT family is largely unknown.

174 In contrast, sole modification of anion channel opening and closing is insufficient to acc

175 capacity glutamate transport system, with an anion channel optimized for anion conduction in the nega

176 ase, which did not contain voltage-dependent anion channel or adenine nucleotide translocator, were r

177 s are sufficient for ABA activation of SLAC1 anion channels or whether additional components are requ

178 d by a piggyback internalization (through an anion channel) or the contribution of labile complexes.

179 ST1) and ultimately results in activation of anion channels, osmotic water loss, and stomatal closure

180 wo major anions and their permeation through anion channels plays essential roles in our body.

181 to study and compare glutamate transport and anion channel properties of both EAAT isoforms.

182 -triphosphate receptor and voltage-dependent anion channel protein expression and elevated the number

183 ial localization of HK2 at voltage-dependent anion channels provides access to ATP generated by oxida

184 ent studies implicate the plasmodial surface anion channel (PSAC) and a role in parasite nutrient acq

185 ients, as mediated by the plasmodial surface anion channel (PSAC) and recently linked to parasite cla

186 The plasmodial surface anion channel (PSAC) increases erythrocyte permeability

187 The plasmodial surface anion channel (PSAC) is an unusual small-conductance ion

188 The plasmodial surface anion channel (PSAC) may mediate these changes.

189 The plasmodial surface anion channel (PSAC) mediates this transport and is an a

190 The plasmodial surface anion channel (PSAC), an unusual voltage-dependent ion c

191 The plasmodial surface anion channel (PSAC), recently identified with electroph

192 athways (NPP) including a Plasmodium surface anion channel (PSAC).

193 lutamate is primarily released by opening of anion channels rather than exocytosis.

194 EAAT anion channels regulate neuronal excitability, and gain-

195 e previously reported that SLAC1, an outward anion channel required for stomatal closure, was regulat

196 The AtQUAC1, an R-type anion channel responsible for the release of malate from

197 ucleotide translocator and voltage-dependent anion channel, resulting in dissipation of mitochondrial

198 d, the first for any eukaryotic ligand-gated anion channel, revealing a macrocyclic lactone-binding s

199 We describe anion channel rhodopsins (ACRs), a family of light-gated

200 basis of the anion specificity of SLAC/SLAH anion channels seems to be determined by the presence an

201 the opening of the SnR kinase OST1-activated anion channel SLAC1 [3, 4].

202 Activation of the guard cell S-type anion channel SLAC1 is important for stomatal closure in

203 OST1 with the inward K(+) channel KAT1, the anion channel SLAC1, and the NADPH oxidases AtrbohD and

204 vating specific ion channels, such as a slow-anion channel (SLAC1) that, in turn, mediate ion efflux

205 phosphorylation and activation of the S-type anion channel SLAH3 by CPK21.

206 a(2+)-dependent CPK2/CPK20 regulation of the anion channel SLAH3 to regulate PT growth.

207 The Arabidopsis thaliana shoot expresses the anion channel SLOW ANION CHANNEL1 (SLAC1) and its homolo

208 ch several states are connected to branching anion channel states.

209 ant ion channels, for example, ALMT and SLAC anion channel subunits, are unique.

210 uli can modulate the ion selectivity of some anion channels, such as CFTR, ANO1 and the glycine recep

211 ological and computational analyses of major anion channels, such as cystic fibrosis transmembrane co

212 host defence defect to the loss of CFTR, an anion channel that facilitates HCO(3)(-) transport.

213 the ubiquitously expressed vertebrate Cl(-) /anion channel that is composed of proteins belonging to

214 SLAC1 encodes a central guard cell S-type anion channel that mediates ABA-induced stomatal closure

215 CFTR is an apical membrane anion channel that regulates fluid homeostasis in many o

216 Thus, a melanosomal anion channel that requires OCA2 is essential for skin a

217 ctance regulator (CFTR) is a plasma-membrane anion channel that, when mutated, causes the disease cys

218 resistance proteins (MRPs), and an ATP-gated anion channel, the cystic fibrosis transmembrane conduct

219 min protein family includes Ca(2+)-activated anion channels (TMEM16A, TMEM16B), a cation channel (TME

220 the ion selectivity of an inhibitory LGC-55 anion channel to an excitatory LGC-55 cation channel.

221 Because trafficking of voltage-dependent anion channel to the cell surface is associated with hea

222 was co-localized with the voltage-dependent anion channel to the mitochondria.

223 Similarly uncertain is the contribution of anion channels to the myogenic response and physiologica

224 Unitary current amplitudes of EAAT5 anion channels turned out to be approximately twice as h

225 tance regulator (CFTR), a cAMP/PKA-activated anion channel, undergoes efficient apical recycling in p

226 that resulted in block of voltage-dependent anion channel (VDAC) "rescued" mitochondrial membrane po

227 e mitochondria through the voltage-dependent anion channel (VDAC) and/or adenine nucleotide transport

228 ion transport through the voltage-dependent anion channel (VDAC) because this channel provides prima

229 ial outer membrane protein voltage-dependent anion channel (VDAC) blocks traffic through the channel

230 The voltage-dependent anion channel (VDAC) constitutes the major pathway for t

231 The voltage-dependent anion channel (VDAC) governs the free exchange of ions a

232 d the mitochondrial marker voltage-dependent anion channel (VDAC) have various expression levels in d

233 The voltage-dependent anion channel (VDAC) in the outer membrane of mitochondr

234 e outer membrane-localized voltage-dependent anion channel (VDAC) is a known Ca(2+) permeability path

235 The voltage-dependent anion channel (VDAC) is the major pathway for ATP, ADP,

236 The voltage-dependent anion channel (VDAC) is the major pathway mediating the

237 The voltage-dependent anion channel (VDAC) is the most abundant protein in the

238 The voltage-dependent anion channel (VDAC) mediates and gates the flux of meta

239 The voltage-dependent anion channel (VDAC) mediates trafficking of small molec

240 espiration by blocking the voltage-dependent anion channel (VDAC) of mitochondrial outer membrane.

241 Reversible blockage of the voltage-dependent anion channel (VDAC) of the mitochondrial outer membrane

242 shown to interact with the voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane

243 echanism was identified as voltage-dependent anion channel (VDAC) oligomerization.

244 Voltage-dependent anion channel (VDAC) proteins are major components of th

245 in the phosphorylation of voltage-dependent anion channel (VDAC) through a protein kinase Cepsilon (

246 the mitochondrial membrane voltage-dependent anion channel (VDAC) via a hydrophobic interaction that

247 The voltage-dependent anion channel (VDAC), a major pore-forming protein in th

248 nslational modification of voltage-dependent anion channel (VDAC), a membrane channel and NADH oxidas

249 n mouse LGN, including the voltage-dependent anion channel (VDAC), adenine nucleotide translocator (A

250 (TFAM), citrate synthase, voltage-dependent anion channel (VDAC), and cytochrome c oxidase subunit 4

251 outer membrane through the voltage-dependent anion channel (VDAC), comprising three isoforms--VDAC1,

252 mitochondrial protein, the voltage-dependent anion channel (VDAC), is implicated in the control of ap

253 rial membrane protein, the voltage-dependent anion channel (VDAC), is increasingly implicated in the

254 e has accumulated that the voltage-dependent anion channel (VDAC), located on the outer membrane of m

255 gulation, dependent on the voltage-dependent anion channel (VDAC), the major channel of MOM, remains

256 -syn reversibly blocks the voltage-dependent anion channel (VDAC), the major channel of the mitochond

257 the metabolite transporter voltage-dependent anion channel (VDAC), the protein translocator of the ou

258 t is co-localized with the voltage-dependent anion channel (VDAC), which is also a t-PA-binding prote

259 (2+) exchange, through the voltage-dependent anion channel (VDAC)-1/glucose-regulated protein 75 (Grp

260 ion decreased the level of voltage-dependent anion channel (VDAC).

261 synthetase (ACSL) and the voltage-dependent anion channel (VDAC).

262 and function of the human voltage dependent anion channel (VDAC-1) as an example of a polytopic inte

263 previously that closure of voltage-dependent anion channels (VDAC) in the mitochondrial outer membran

264 The voltage-dependent anion channels (VDAC) were identified as components of M

265 , ATP, ADP, and Pi through voltage-dependent anion channels (VDAC).

266 , cardiolipin content, and voltage-dependent anion channel [VDAC] content) as well as Q(10) content w

267 SOD1 binds directly to the voltage-dependent anion channel (VDAC1), an integral membrane protein imbe

268 Voltage-dependent anion channels (VDACs) are a family of small pore-formin

269 In mammals, the Voltage-dependent anion channels (VDACs) are predominant proteins of the o

270 Voltage-dependent anion channels (VDACs) are the most abundant proteins in

271 whether mitophagy, through voltage dependant anion channels (VDACs) interacting with microtubule-asso

272 acts through mitochondrial voltage-dependent anion channels (VDACs)--a novel target for anti-cancer d

273 Volume-regulated anion channel (VRAC) activity was assessed from conventi

274 yric acid (DCPIB), a potent volume-regulated anion channel (VRAC) inhibitor, suppresses pathological

275 KEY POINTS: The volume-regulated anion channel (VRAC) is a swelling-activated chloride ch

276 The volume-regulated anion channel (VRAC) is activated when a cell swells, an

277 ABSTRACT: The volume-regulated anion channel (VRAC) is the ubiquitously expressed verte

278 Activation of a ubiquitous volume-regulated anion channel (VRAC) plays a key role in this process; h

279 essential component of the volume-regulated anion channel (VRAC), which controls cellular volume.

280 uitously expressed volume-regulated chloride/anion channel (VRAC).

281 ss results in activation of volume-regulated anion channels (VRAC) that drive a compensatory regulato

282 as the selective blocker of volume-regulated anion channels (VRAC).

283 Canonical volume-regulated anion channels (VRACs) are crucial for cell volume regul

284 response to cell swelling, volume-regulated anion channels (VRACs) participate in a process known as

285 Volume-regulated anion channels (VRACs) play an important role in control

286 amino acid taurine through volume-regulated anion channels (VRACs), and it has been hypothesized tha

287 s as a volume-sensitive outwardly rectifying anion channel (VSOAC) in some cell types.

288 fibrosis transmembrane conductance regulator anion channel was investigated in T84 cells, and in porc

289 the bicarbonate-induced activation of S-type anion channels was reduced in the dominant active PP2C m

290 ,4,5-triphosphate receptor-voltage-dependent anion channel, we revealed that nanomolar concentrations

291 and 4.2 also bind to band 3, the erythrocyte anion channel, we suggest that one or both of these prot

292 directly modifies the opening/closing of the anion channel, we used voltage clamp fluorometry.

293 ative potentials open probabilities of EAAT5 anion channels were much larger than for GLT-1c.

294 g stomatal opening, by mutation of the SLAC1 anion channel, which mediates solute loss for closure.

295 op1 mutation impaired the activity of S-type anion channels, which are critical for stomatal closure.

296 Cytosolic Ca(2+) activation of S-type anion channels, which play a central role in Ca(2+)-reac

297 ansmembrane conductance regulator (CFTR), an anion channel whose dysfunction leads to chronic bacteri

298 s suggest that EAAT5 behaves as a slow-gated anion channel with little glutamate transport activity.

299 Anion channels with 10-picosiemen conductance are also p

300 spholipid bilayers, form constitutively open anion channels with extreme selectivity for F(-) over Cl