ライフサイエンスコーパス: anion channel

1 hat functions as a phosphorylation-regulated anion channel.

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

3 s transmembrane conductance regulator (CFTR) anion channel.

4 s transmembrane conductance regulator (CFTR) anion channel.

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

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

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

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

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

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

11 fibrosis transmembrane conductance regulator anion channel.

12 s transmembrane conductance regulator (CFTR) anion channel.

13 udies strongly suggest that EcYfdC is not an anion channel.

14 like cytoplasmic kinase PBL27, and the SLAH3 anion channel.

15 s Transmembrane Conductance Regulator (CFTR) anion channel.

16 that underpin evolution from transporter to anion channel.

17 ant OMM transporter is the voltage-dependent anion channel.

18 d unitary current amplitudes in mutant EAAT2 anion channels.

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

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

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

22 described, this is most likely based on fast anion channels.

23 ased absolute open probability of L46P EAAT2 anion channels.

24 nducting) converted into chloride-conducting anion channels.

25 gle-channel current amplitudes of associated anion channels.

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

27 glutamate transporters but also function as anion channels.

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

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

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

31 the first identified auxiliary subunits for anion channels.

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

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

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

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

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

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

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

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

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

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

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 ial membrane (OMM) protein voltage-dependent anion channel 1 (VDAC1).

46 ondrial membrane channels, voltage-dependent anion channel 1 and the mitochondrial calcium uniporter,

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

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

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

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

51 nductive pathway involving voltage-dependent anion channel-1 (VDAC-1) and by exocytosis of ATP locali

52 lls with inhibitors of the voltage-dependent anion channel-1 (VDAC-1) or treatment with a VDAC-1 sele

53 a, INSR interacts with the voltage-dependent anion channel-1 (VDAC1) in mitochondria and that INSR kn

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

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

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

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

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

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

60 as connexins, innexins and volume-regulated anion channels(4-8).

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

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

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

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

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

66 transduction module from MAMP recognition to anion channel activation, and independent of ABA-induced

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

68 gulation of ATP release and volume-regulated anion channel activity and provide critical links among

69 rtially rescues the defective processing and anion channel activity conferred by the major cystic fib

70 Whereas anion channel activity has been extensively investigated

71 Anion channel activity is known to depend on phosphoryla

72 nchoe fedtschenkoi, we found that guard cell anion channel activity, recorded under voltage clamp, fo

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

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

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

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

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

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

79 Anion channels and antiporters of the ClC superfamily ha

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

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

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

83 Eukaryotic CLC anion channels and transporters are homodimeric proteins

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

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

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

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

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

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

90 Anion channels are a putative path for P(i) into the SR.

91 CLC anion channels are homodimeric proteins.

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

93 cular carriers for anions and supramolecular anion channels are reviewed followed by an overview of t

94 Here, using the human voltage-dependent anion channel as our template scaffold, we designed and

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

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

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

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

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

100 L46 is a pore-forming residue of the EAAT2 anion channels at the cytoplasmic entrance into the ion

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

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

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

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

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

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

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

108 ces currents mediated via slow-type (S-type) anion channels by a yet not understood mechanism.

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

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

111 Activation of these GABA receptor anion channels can depolarize horizontal cells and incre

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

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

114 3',5'-cyclic monophosphate (cAMP)-activated anion channel CFTR mediates Cl(-)-dependent fluid secret

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

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

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

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

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

120 cholesterol levels control volume-regulated anion channel-dependent ATP release.

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

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

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

124 nisms, plausibly including Mal activation of anion channels, ensure closure in the light.

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

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

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

128 ipulation of horizontal cells with exogenous anion channel expression mimics GABA-mediated cone CaV c

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

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

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

132 uantify absolute open probabilities of EAAT2 anion channels from ratios of anion currents by glutamat

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

134 s proteasomal degradation, extinguishing its anion channel function.

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

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

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

138 This particular anion channel gating mechanism predicts the existence of

139 anion pore and demonstrate the existence of anion channel gating processes outside the EAAT uptake c

140 We conclude that the diurnal cycle of anion channel gene transcription, rather than the physio

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

144 d highlight the importance of the LRRC8/VRAC anion channel in cell differentiation.

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

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

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

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

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

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

151 osmotic conditions activate volume-regulated anion channels in vertebrate cells.

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

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

154 articipate at neutral pH values, because the anion channel inhibitor 5-nitro-2-(3-phenylpropylamino)

155 ne product bestrophin-1, a Ca(2+) -dependent anion channel, interacts with Ca(V) 1.3 Ca(2+) channels

156 MVID, decreased surface expression of apical anion channels involved in Cl(-) extrusion, such as cyst

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

158 s Transmembrane Conductance Regulator (CFTR) anion channel is essential for epithelial salt-water bal

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

160 s transmembrane conductance regulator (CFTR) anion channel is the most frequent mutation causing cyst

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

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

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

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

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

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

167 r counterparts of the scrambling-incompetent anion channel mTMEM16A, yet with distinct differences in

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

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

170 e lateral movement of this domain results in anion channel opening.

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

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

173 fibrosis transmembrane conductance regulator anion channels or proinflammatory cytokines might alter

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

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

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

177 xpressed acid-sensitive outwardly-rectifying anion channel PAORAC/ASOR.

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

179 s transmembrane conductance regulator (CFTR) anion channels produced submucosal gland mucus that was

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

181 xistence of mutant transporters with changed anion channel properties, but without alteration in glut

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

183 chondrial DNA content, and voltage-dependent anion channel protein expression.

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

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

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

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

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

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

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

191 EAAT anion channels regulate neuronal excitability, and gain-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 (2019) show that the volume-regulated anion channel Swell1 in astrocytes mediates the release

208 nductance regulator (CFTR) gene, encoding an anion channel that conducts chloride and bicarbonate acr

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

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

211 tance regulator (CFTR) is an apical membrane anion channel that is widely expressed in epithelia thro

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

213 ctance regulator (CFTR) is a plasma membrane anion channel that plays a key role in controlling trans

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

215 rc8a) functionally encodes a swell-activated anion channel that regulates PI3K-AKT, ERK1/2, mTOR sign

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

222 Here, we examined the contribution of anion channels to cGAMP transfer and anti-viral defense.

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

224 and AcDct(p) into the voltage-dependent slow-anion channel transporter (SLAC1) clade of transporters,

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

226 ter increase ATP release by volume-regulated anion channels under hypotonic conditions.

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

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

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

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

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

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

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

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

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

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

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

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

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

240 ts via pores formed by the voltage-dependent anion channel (VDAC) oligomers in the mitochondrial oute

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

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

243 A structure of the murine voltage-dependent anion channel (VDAC) was determined by microcrystal elec

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

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

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

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

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

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

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

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

252 opore of the mitochondrial voltage-dependent anion channel (VDAC), reconstituted into planar bilayers

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

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

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

256 (2+) exchange, through the voltage-dependent anion channel (VDAC)-1/glucose-regulated protein 75 (Grp

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

258 anslocase (ANT) and of the voltage-dependent anion channel (VDAC).

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

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

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

262 robe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide

263 factor (MFF1 and MFF2) and voltage-dependent anion channel (VDAC1) as a novel regulator of mitochondr

264 ptosis activator, binds to voltage-dependent anion channels VDAC2 and VDCA3, but treatment with erast

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

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

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

268 egulator) gene that encodes a cAMP-dependent anion channel vital for proper Cl(-) and HCO(3)(-) trans

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

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

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

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

273 Volume-regulated anion channel (VRAC) is the chloride channel that is act

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

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

276 containing family 8 (LRRC8)/volume-regulated anion channel (VRAC) promotes mouse myoblast differentia

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

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

279 ugh the glutamate-permeable volume-regulated anion channel (VRAC).

280 aracterized the key role of volume-regulated anion channels (VRAC) in the modulation of the volume of

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

282 , an essential component of volume-regulated anion channels (VRAC), as a vital regulator of hypotonic

283 c channels, better known as volume-regulated anion channels (VRAC), as widely expressed cGAMP transpo

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

285 Volume-regulated anion channels (VRACs) are central to cell volume regula

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

287 Volume-regulated anion channels (VRACs) are key players in regulatory vol

288 revealed that inhibition of volume-regulated anion channels (VRACs) increased propagation of the DNA

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

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

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

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

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

294 ,4,5-triphosphate receptor-voltage-dependent anion channel, we revealed that nanomolar concentrations

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

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

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

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

299 ta anion channelrhodopsin 1 is a light-gated anion channel widely used as an optogenetic inhibitory t

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