ライフサイエンスコーパス: Ano1

1 Ca(2+)-activated Cl(-) channel anoctamin 1 (ANO1).

2 teases, calpain 14 (CAPN14) and anoctamin 1 (ANO1).

3 ished following blockade of either Cav(L) or ANO1.

4 ntracellular trafficking, or localization of ANO1.

5 dy of the structure-function relationship of ANO1.

6 eticulum-associated, proteasomal turnover of ANO1.

7 ess mRNA for a previously unknown variant of Ano1.

8 lower kinetics compared with the full-length Ano1.

9 nts to determine the quaternary structure of Ano1.

10 e first to probe the quaternary structure of Ano1.

11 oxious heat sensor TRPV1, which can activate ANO1.

12 erize PI(4,5)P(2) binding modes and sites on ANO1.

13 that pharmacological inhibition of TMEM16A (ANO1), a calcium-activated chloride channel expressed in

14 Ca(2+) release in ICC-IM activates Ano1, a Ca(2+) -activated Cl(-) conductance, causing tis

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

16 ANO1, a calcium-activated chloride channel, is highly ex

17 , yet our understanding of the mechanisms of ANO1 activation and regulation are only beginning to eme

18 Enhancing ICC-IM Ca(2+) release and Ano1 activation contributes to excitatory responses of c

19 oupling may represent a general mechanism of ANO1 activation in native tissues.

20 HTR2B or ANO1 activation is sufficient for urethral contraction a

21 sensitivity of ANO1 and hence in regulating ANO1 activation.

22 ) release, which may be necessary to enhance ANO1 activation.

23 serves as an adjunct to other mechanisms of ANO1 activation.

24 ation, we used pharmacological inhibitors of Ano1 activity and shRNA-mediated knock down of Ano1 expr

25 echanism of channel gating and regulation of ANO1 activity.

26 I cells and their dependence upon Cav(L) and ANO1 all suggest that these cells are viable candidates

27 tivated chloride channel (CaCC) anoctamin 1 (ANO1, also known as TMEM16A).

28 Ca(2+)-activated Cl(-) channel, anoctamin 1 (Ano1, also known as transmembrane protein 16A) contribut

29 Knockdown of ANO1 in ANO1-amplified breast cancer cell lines and other cancer

30 targeting approach for antitumor therapy in ANO1-amplified cancers.

31 bitor CaCCinh-A01 decreases proliferation of ANO1-amplified cell lines; however, the mechanism of act

32 Ano1 and Cacna1c expression levels were examined by quan

33 and tone in the IAS were nearly abolished by ANO1 and CavL antagonists.

34 We propose that ANO1 and CavL collaborate to generate SWs in ICC-IM foll

35 ane potential and contraction indicated that ANO1 and CavL have a central role in SW generation, phas

36 These data support a central role for ANO1 and CavL in the generation of SWs and tone in the I

37 ationship between expression and function of ANO1 and esophageal epithelial proliferation in patients

38 ce impairs receptor-stimulated activation of ANO1 and fluid secretion.

39 Ion selectivity of CFTR, ANO1 and GlyR is critically affected by the electric per

40 rbonate permeability (P HC O3/ Cl ) of CFTR, ANO1 and GlyR.

41 coupling calcium and voltage sensitivity of ANO1 and hence in regulating ANO1 activation.

42 or a better understanding of the function of ANO1 and its role in health and diseases.

43 tivity of some anion channels, such as CFTR, ANO1 and the glycine receptor (GlyR), by changing pore s

44 IM were the predominant cell type expressing ANO1 and the most likely candidate for SW generation.

45 Recently, TMEM16A (ANO1) and -B were shown to be critical components of CaC

46 s to be functionally characterized, TMEM16A (ANO1) and TMEM16B (ANO2), form Ca(2+)-activated Cl(-) ch

47 Anoctamin 1 (ANO1) and transmembrane Protein 147 (TMEM147), both in n

48 oth activities are dependent on anoctamin 1 (ANO1) and voltage-dependent Ca(2+) channels (VDCCs).

49 -activated Cl(-) channels (ANO1, encoded by Ano1) and voltage-dependent L-type Ca(2+) channels (CavL

50 Ca(2+) -activated Cl(-) channels (encoded by Ano1) and voltage-dependent L-type Ca(2+) channels (enco

51 lear SCs, including Tectb, Cyp26b1, Slitrk6, Ano1, and Aqp4.

52 Ca(2+) -activated Cl(-) channels, encoded by Ano1, and rely upon this conductance for physiological f

53 By analyzing ANO1-ANO6 chimeric proteins, we identify a domain in ANO

54 e potential of colonic tissues as a specific Ano1 antagonist hyperpolarized colonic muscles by ~10 mV

55 ANO1 antagonists also abolished SWs as well as transient

56 Comparison of the effects of Ano1 antagonists on muscles from juvenile and adult smal

57 scles, and the sensitivity of contraction to ANO1 antagonists was the same in stretched versus un-str

58 Ano1 antagonists, benzbromarone and Ani9 inhibited the e

59 Several transcripts for Ano1 are generated by alternative splicing of four exons

60 ver, the mechanisms underlying regulation of Ano1 are unknown.

61 Anoctamin-1 Ca(2+)-activated Cl(-) channels (ANO1) are proposed to modulate contractility of urethra

62 th 11q13 amplification, thereby establishing ANO1 as a promising target for therapy in these highly p

63 We find that Ano1 associates with the signaling/scaffolding proteins

64 co-localize with other ICC markers CD34 and Ano1, but not with mast cell marker tryptase.

65 We conclude that Gli1 and Gli2 repress ANO1 by a novel mechanism that is independent of Gli cle

66 es provide new perspectives on regulation of Ano1 by Ca2+.

67 y modulate the anion selectivity of CFTR and ANO1 by changing the pore size.

68 he activity of the CaCC TMEM16A/Anoctamin 1 (ANO1) by directly engaging the channel at the cell surfa

69 x, that phosphorylates ANO1 S673, increasing ANO1 Ca(2+) affinity.

70 phorylates ANO1 S221, which markedly reduces ANO1 Ca(2+) affinity.

71 ) and is explained by a stabilization of the ANO1 Ca(2+)-bound open state.

72 Ano1, Cacna1c and Kit gene expression were the same in e

73 reased ANO1 calcium sensitivity and rendered ANO1 calcium gating voltage-independent, demonstrating a

74 Mutations such as S741T increased ANO1 calcium sensitivity and rendered ANO1 calcium gatin

75 Ano1 can be gated by Ca(2+) or by voltage in the absence

76 An Ano1 channel antagonist inhibited intercellular Ca(2+) w

77 ntractions induced by EFS were reduced by an Ano1 channel antagonist, abolished by DAU 5884, and unaf

78 we revealed an intricate mechanism of TRPV1-ANO1 channel coupling in rat dorsal root ganglion (DRG)

79 ension of TM6, which plays a crucial role in ANO1 channel gating, and increases the accessibility of

80 ce of the membrane allosterically regulating ANO1 channel gating.

81 However, a specific ANO1 channel inhibitor, Ani9, failed to affect urethral

82 ometric protein networks associated with the Ano1 channel.

83 These are similar in conductance to ANO1 channels (8 pS) expressed in HEK293 cells.

84 Ca(2+) transients and sustains activation of ANO1 channels and depolarization during slow waves.

85 ICC-SS express Ano1 channels and generate spontaneous Ca(2+) transients

86 Ca(2+) transients, through activation of Ano1 channels and generation of inward current, cause ne

87 Ano1 channels are activated by Ca(2+) release from the e

88 Ano1 channels are expressed by interstitial cells of Caj

89 Release of Ca(2+) and activation of Ano1 channels causes depolarization of ICC-SS and LSMC,

90 Spontaneous Ca(2+) transients activate Ano1 channels in ICC-SS.

91 uch events have been linked to activation of Ano1 channels in ICC.

92 Recent findings indeed indicate that ANO1 channels often co-localize with sources of intracel

93 Recent findings indeed indicate that ANO1 channels often co-localize with sources of intracel

94 elease in ICC limits the open probability of Ano1 channels, reducing the excitability of electrically

95 results from suppression of the activity of Ano1 channels, which are expressed exclusively in inters

96 intracellular Ca(2+) transients towards the ANO1 channels.

97 us intracellular Ca2+ transients towards the ANO1 channels.

98 are dependent on activation of anoctamin 1 (ANO1) channels in interstitial cells of Cajal (ICC), we

99 Moreover, ANO1 chloride channel activity was important for cell vi

100 Our results highlight the involvement of the ANO1 chloride channel in tumor progression and provide i

101 pid-interacting proteins are enriched in the Ano1 complex.

102 Thus, utilizing mCherry- and eGFP-tagged Ano1 constructs, we conducted biochemical and Forster re

103 Together, our data reveal the existence of ANO1-containing multichannel nanodomains in DRG neurons

104 Amplification of ANO1 correlated with disease grade and poor prognosis.

105 embrane-cytosol interface found 3 regions of ANO1 critical for PI(4,5)P(2) regulation that correspond

106 oreover, interfering RNA for moesin modifies Ano1 current without affecting its surface expression le

107 C-IM are the probable cellular candidate for ANO1 currents and SW generation.

108 ANO1 currents in excised inside-out patches activated by

109 Ca(2+) signalling in ICC activates ANO1 currents in ICC.

110 In addition, Ani9 inhibited ANO1 currents recorded in HEK 293 cells, at concentratio

111 ANO1 protein levels in these cells, whereas ANO1 currents were still inhibited by CaCCinh-A01, indic

112 to describe inhibitors capable of promoting ANO1 degradation and report new inhibitors of ANO1-depen

113 not sufficient to diminish proliferation of ANO1-dependent cancer cells.

114 ctivity of ANO1 is not sufficient to inhibit ANO1-dependent cell proliferation, indicating that the r

115 NO1 degradation and report new inhibitors of ANO1-dependent cell proliferation.

116 the esophageal epithelium, and that loss of ANO1-dependent Cl(-) transport abrogated esophageal epit

117 Mechanistically, ANO1-dependent regulation of basal cell proliferation wa

118 Loss of function of ANO1 did not inhibit the development of ICC networks tha

119 ydryl reagents alter the Ca2+ sensitivity of Ano1 E702C and E705C as expected if E702 and E705 are in

120 ANO1 expression was examined in wildtype and Ano1(/+egfp) mice with immunohistochemical techniques.

121 unction of a new class of CaCC, anoctamin 1 (ANO1), encoded by Tmem16a, which was discovered to be hi

122 ivation of Ca(2+) -activated Cl(-) channels (ANO1, encoded by Ano1) and voltage-dependent L-type Ca(2

123 etween transcription initiation sites in the ANO1 enhancer and FGF3 promoter that quantitatively scal

124 romobility shift assays, which revealed that Ano1 exists as a dimer.

125 Knockdown of ANO1 expression caused decreased insulin secretion in hu

126 Dual labelling revealed that ANO1 expression could be resolved in ICC but not smooth

127 We observed increased ANO1 expression in esophageal biopsy samples from patien

128 Changes in Ano1 expression in ICC may directly contribute to diabet

129 o1 activity and shRNA-mediated knock down of Ano1 expression in organotypic cultures of Ano1 WT small

130 results help elucidate the critical role of ANO1 expression in prostate cancer bone metastases, whic

131 o glucose, this contact was strengthened and ANO1 expression increased, whereas inhibition of INS gen

132 While ANO1 expression negatively correlates with survival in s

133 Knocking down Ano1 expression using Cre/LoxP technology caused dramati

134 ed with fluorescence-activated cell sorting, Ano1 expression was 26.5-fold greater in ICC than in SMC

135 ANO1 expression was examined in wildtype and Ano1(/+egfp

136 t feedback loop involving INS transcription, ANO1 expression, and insulin secretion.

137 Treatment with a known regulator of Ano1 expression, IL-4, increased promoter activity by 1.

138 found three CpG islands that correlated with ANO1 expression, including two positively correlated wit

139 on by INS promoter targeting siRNA decreased ANO1 expression, revealing a regulatory effect of INS pr

140 rrelated with but not sufficient to increase ANO1 expression, suggesting methylation of positively co

141 aling a regulatory effect of INS promoter on ANO1 expression.

142 nmental cadmium contributes significantly to ANO1 expression.

143 ositively correlated CpG islands potentiates ANO1 expression.

144 ly correlated CpG island without a change in ANO1 expression.

145 Ano1, ezrin, and moesin/radixin colocalize apically in s

146 ized information about mechanisms regulating Ano1 function and trafficking to polarized domains of th

147 haracteristics, providing new tools to study ANO1 function in biological systems, paving the path for

148 rationale for pharmacologic intervention of ANO1 function in patients with EoE.

149 We show that inhibition of ANO1 function is not sufficient to diminish proliferatio

150 TMEM16A (ANO1) functions as a calcium-activated chloride channel

151 d Tmem16) superfamily, but the mechanisms of Ano1 gating by Ca2+ remain enigmatic.

152 anscripts encoded by alternative splicing of Ano1 gene in gastric muscles of patients with diabetic g

153 gion near the insulin (INS) promoter and the ANO1 gene, lying 68 Mb away on human chromosome 11, whic

154 Direct repression of anoctamin 1 (ANO1) gene transcription by Gli proteins.

155 In conclusion, Ano1 has a previously unidentified role in the regulatio

156 Activation of ANO1 has been shown to generate spontaneous transient in

157 dependent chloride channel TMEM16A (TAOS2 or ANO1) has been reported in several malignancies.

158 -activated chloride conductance anoctamin-1 (Ano1) has been shown to be responsible for the generatio

159 gastric corpus muscles showed that c-KIT(+)/ANO1(+) ICC-IM and PDGFRalpha(+) cells were closely appo

160 Knockdown of ANO1 in ANO1-amplified breast cancer cell lines and othe

161 l proliferation, indicating that the role of ANO1 in cancer only partially depends on its function as

162 We examined mRNA and protein expression of ANO1 in esophageal biopsy samples from patients with EoE

163 These data identify a functional role for ANO1 in esophageal cell proliferation and BZH in patient

164 lial cells, and overexpression of moesin and Ano1 in HEK cells alters the subcellular localization of

165 Overexpression of Ano1 in HEK cells or Xenopus oocytes is sufficient to ge

166 sduced by PDGFRalpha(+) cells, can influence ANO1 in ICC is unknown.

167 To explore a possible role of ANO1 in insulin metabolism, we carried out experiments i

168 Genetic deletion of Ano1 in mice resulted in loss of slow waves in smooth mu

169 reveal critical and non-redundant roles for Ano1 in organogenesis, and show that chloride channels a

170 ortant changes in expression and splicing of Ano1 in patients with diabetic gastroparesis that alter

171 ws deeper understanding of the regulation of Ano1 in physiology and as a potential therapeutic target

172 ese data demonstrate the fundamental role of ANO1 in the generation of slow waves in GI ICC.

173 To confirm the role of Ano1 in the loss of Ca(2+) transient coordination, we us

174 lcium-activated chloride channel anoctamin1 (ANO1) in cancer metastasis, its direct impact on the met

175 cium-activated chloride channel anoctamin 1 (ANO1) in esophageal proliferation and the histopathologi

176 ated chloride channel TMEM16A, also known as ANO1, in VSMCs, intermediate cells, and pericytes elimin

177 Another network associated with Ano1 includes the SNARE and SM proteins VAMP3, syntaxins

178 post-spike notch, which was exaggerated with ANO1 inhibition, and significantly increased the peak po

179 The ANO1 inhibitor CaCCinh-A01 decreases proliferation of AN

180 s to elucidate novel biological functions of ANO1 inhibitors.

181 The objective was to identify regions of Ano1 involved in channel gating by Ca2+.

182 ssociates the ANO1-VAPA interaction, forming ANO1-IRBIT-E-Syt2-AC6-AKAP11-PKA complex that phosphoryl

183 ANO1 is a calcium-activated chloride channel that is fre

184 BK channels are activated when ANO1 is absent or blocked and slightly impair contractil

185 ANO1 is activated by elevation of cytosolic Ca(2+) and m

186 We have found that ANO1 is amplified and highly expressed in breast cancer

187 Whether ANO1 is amplified in breast tumors, the extent to which

188 Understanding the oligomeric nature of Ano1 is an essential step in the development of therapeu

189 For example, Ano1 is highly expressed in multiple tissues including a

190 ANO1 is implicated as a potential target to treat incont

191 verexpression, and whether overexpression of ANO1 is important for tumor maintenance have remained un

192 Here, we show that ANO1 is minimally expressed in LNCap and DU145 prostate

193 e that inhibition of the channel activity of ANO1 is not sufficient to inhibit ANO1-dependent cell pr

194 Ano1 is overexpressed in cancer.

195 estingly, it appears that in many cell types ANO1 is particularly tightly coupled to the Ca(2+) relea

196 estingly, it appears that in many cell types ANO1 is particularly tightly coupled to the Ca2+ release

197 Ca(2+) sensitivity of ANO1 is rather low and at negative membrane potentials t

198 Ca2+ sensitivity of ANO1 is rather low and at negative membrane potentials t

199 In this study, we show that Ano1 is required to maintain coordinated Ca(2+) transien

200 e approaches, supporting the conclusion that Ano1 is required to maintain coordination/rhythmicity of

201 of expression after IL-13 stimulation, that ANO1 is the primary apical IL-13-induced Cl(-) transport

202 TMEM16A (ANO1) is a calcium-activated chloride channel (CaCC) exp

203 Anoctamin-1 (Ano1) is a widely expressed protein responsible for endo

204 cium-activated chloride channel anoctamin 1 (ANO1) is located within the 11q13 amplicon, one of the m

205 TMEM16A (also known as anoctamin 1, ANO1) is thought to function as the Ca(2+) activated sec

206 tein 16A (TMEM16A), also called anoctamin 1 (ANO1), is a calcium-activated chloride channel expressed

207 that the calcium-activated chloride channel, ANO1, is expressed by pacemaker cells and may contribute

208 Mice homozygous for Ano1 knock-out exhibit abnormal ICC function and motilit

209 Mechanistically, ANO1 knockdown or pharmacological inhibition of its chlo

210 atiotemporal maps of contractile activity in Ano1 KO and WT tissues.

211 n-rhythmic and uncoordinated was observed in Ano1 KO jejunum.

212 (2+) transients within the ICC-MY network in Ano1 KO mice were uncoordinated, while ICC-MY Ca(2+) tra

213 proteins transmembrane protein 16A (TMEM16A, ANO1), leucine-rich repeat (LRR)-containing 8 (LRRC8), C

214 ANO1 limits the peak membrane potential achieved in the

215 es suggests that conductances in addition to Ano1 may develop with age and contribute to pacemaker ac

216 Voltage-dependent gating of Ano1 measured in the presence of intracellular Ca(2+) wa

217 high-fat diet-fed Ano1(+/-) mice relative to Ano1(+/+) mice fed the same diet.

218 sulin-to-glucose ratios in high-fat diet-fed Ano1(+/-) mice relative to Ano1(+/+) mice fed the same d

219 in metabolism, we carried out experiments in Ano1(+/-) mice.

220 mpetus for gaining a deeper understanding of ANO1 modulation in cells and introduce a new targeting a

221 unctionally characterized approximately 6000 ANO1 mutants and identified novel mutations that affecte

222 The novel ANO1 mutants reported have diverse functional characteri

223 Mouse Ano1(-/-)mutants exhibited mucus obstruction and abnorma

224 n be defined by the presence of c-Kit, CD34, Ano1, NTPDase2, connexin 43, vimentin, desmin, PDGFbeta

225 juvenile animals in which effects of reduced Ano1 on gastric emptying and motor patterns could not be

226 Deficiency in Ano1 or Gardos channel did not reduce platelet responses

227 activated Cl(-) channel (CaCC), Anoctamin 1 (Ano1 or TMEM16A), has been implicated in vital physiolog

228 ell Ca(2+) transients that were inhibited by ANO1 or VDCC antagonists revealing the underlying asynch

229 terozygous of homozygous deficiency in Ano6, Ano1, or Ca(2+)-dependent KCa3.1 Gardos channel.

230 t to which gene amplification contributes to ANO1 overexpression, and whether overexpression of ANO1

231 nalyses found the families were related, and ANO1 p.Met658Val segregated with moyamoya disease in the

232 in ICC and are consistent with the idea that ANO1 participates in pacemaker activity.

233 (2) Three of these sites captured 85% of all ANO1-PI(4,5)P(2) interactions.

234 ANO1 plays a crucial role in determining numerous physio

235 Quantum chemical calculations (CCSD(T)/ANO1) predict an unsymmetrical equilibrium structure for

236 ANO1 promoter activity was determined using a luciferase

237 This study identifies the Ano1 promoter and defines a mechanism for regulating its

238 The human ANO1 promoter contains binding sites for the glioma-asso

239 ANO1 promoter methylation was also correlated with patie

240 e-wide association studies were used to test ANO1 promoter polymorphisms for association with disease

241 ethylation was detected at the CpG island of ANO1 promoter region in LNCap and DU145 cells, and 5-Aza

242 Hypermethylation of the ANO1 promoter was strongly correlated with but not suffi

243 were used to induce hypermethylation of the ANO1 promoter.

244 Ca(2+) transients not dependent on Cav(L) or ANO1; properties typical of ICC-IM mediating neural resp

245 ANO1 protein is expressed abundantly and specifically in

246 Washout of CaCCinh-A01 rescued ANO1 protein levels and resumed cell proliferation.

247 We report that CaCCinh-A01 reduces ANO1 protein levels by facilitating endoplasmic reticulu

248 Consistently, CaCCinh-A01 failed to reduce ANO1 protein levels in these cells, whereas ANO1 current

249 -A01 inhibits cell proliferation by reducing ANO1 protein levels.

250 The calcium-activated chloride channel ANO1 regulates multiple physiological processes.

251 rovide a comprehensive footprint of putative Ano1 regulatory networks.

252 and suggest that coupling between TRPV1 and ANO1 requires ER Ca(2+) release, which may be necessary

253 tion of Gli activity increased expression of ANO1 RNA and Ca(2+)-activated Cl(-) currents in HEK293 c

254 2-AC6-AKAP11-PKA complex that phosphorylates ANO1 S221, which markedly reduces ANO1 Ca(2+) affinity.

255 1-AC8-AKAP5-PKA complex, that phosphorylates ANO1 S673, increasing ANO1 Ca(2+) affinity.

256 nts on T84 cells, which endogenously express Ano1, showed a 2.1 +/- 0.12-fold increase in binding of

257 noprecipitation studies revealed that tagged Ano1 subunits directly associated before they reached th

258 describe a fundamental dynamic regulation of ANO1 surface expression and Ca(2+)-dependent gating via

259 Ca(2+)-activated Cl(-) channels, encoded by Ano1, that generate inward current, and PDGFRalpha(+) ce

260 embrane protein 16A (TMEM16A), also known as ANO1, the pore-forming subunit of a Ca(2+) -dependent Cl

261 n the muscle layers, ICC selectively express Ano1, thought to underlie classical Ca(2+)-activated Cl(

262 downs of anoctamin-1 in ICC (Kit(CreERT2/+) ;Ano1(tm2jrr/+) ) in GI muscles.

263 Although the founding members ANO1 (TMEM16A) and ANO2 (TMEM16B) are Ca(2+)-activated C

264 Here, we show that conditional deletion of Ano1 (Tmem16a) in mice disrupts Ca(2+) waves within Koll

265 ANO1 (TMEM16A) is a Ca(2+)-activated Cl(-) channel (CaCC

266 ANO1 (TMEM16A) is a Ca(2+)-activated Cl(-) channel that

267 ntly become possible with the discovery that Ano1 (TMEM16a) is an essential subunit of CaCCs.

268 Ano1 (Tmem16a), a Ca(2+)-activated Cl(-) channel, is an

269 Anoctamin-1 (ANO1, TMEM16A) is a principal CaCC subunit in many cell

270 inal acidification and provide evidence that ANO1/TMEM16A acts to attenuate this pH shift.

271 The identification of ANO1/TMEM16A as the likely calcium-dependent chloride ch

272 se, genetic inactivation of chloride channel Ano1/Tmem16a compromises airway barrier function, result

273 asure intraluminal pH and test the idea that ANO1/TMEM16A contributes to luminal pH balance.

274 We conclude that ANO1/TMEM16A is a significant pathway in pancreatic acin

275 ly in ciliogenesis and chloride transport by ANO1/TMEM16A is required for the genesis or maintenance

276 ne conductance regulator (CFTR), anoctamin-1(ANO1/TMEM16A) and the glycine receptor (GlyR), revealed

277 (2+)-activated Cl ((-)) channel anoctamin-1 (ANO1/TMEM16A) is located in the primary cilium and that

278 The calcium-dependent chloride channel DOG1 (ANO1/TMEM16A), which is strongly and specifically expres

279 levels of TRPP1, TRPC1, TRPC3, TRPC6, TRPM4, ANO1/TMEM16A, or voltage-dependent Ca(2+) (CaV1.2) chann

280 We propose an alternative model of Ano1 topology based on mutagenesis, epitope accessibilit

281 Binding and functional effects of Glis on ANO1 transcription and expression were demonstrated by c

282 We investigated regulation of ANO1 transcription by Gli.

283 and Gli2 bound to the promoter and repressed ANO1 transcription.

284 pended on Gli binding to a site close to the ANO1 transcriptional start site.

285 Proximity ligation assays established that ANO1, TRPV1, and the IP(3) receptor IP(3)R1 were often f

286 ial 3-dimensional model system revealed that ANO1 undergoes chromatin modification and rapid upregula

287 By contrast, E-Syt2 dissociates the ANO1-VAPA interaction, forming ANO1-IRBIT-E-Syt2-AC6-AKA

288 omplexes, while E-Syt1 mediates formation of ANO1-VAPA-IRBIT-E-Syt1-AC8-AKAP5-PKA complex, that phosp

289 The Ca2+ sensitivity of Ano1 was estimated from rates of current activation, and

290 Immunolabelling revealed ANO1 was expressed in USMC and not in specialized popula

291 ANO1 was expressed within the esophageal basal zone, and

292 pe Ca(2+) channels (Cav(L)) and anoctamin 1 (ANO1) was tested since each is essential for SW and tone

293 To determine the oligomeric structure of Ano1, we performed chemical cross-linking, non-denaturin

294 SCC datasets with differential expression of ANO1, we showed hypermethylation of positively correlate

295 ANO1 which is a Ca(2+)-activated chloride channel has mu

296 PDGFRalpha(+) cells also express Ano1, which encodes a Ca(2+) -activated Cl(-) conductanc

297 LS and sufficient to confer this function on ANO1, which normally does not scramble.

298 ntaneous Ca(2+) transients in ICC-MY in both Ano1 WT and knockout (KO) mice.

299 ordinated, while ICC-MY Ca(2+) transients in Ano1 WT mice were rhythmic and coordinated.

300 f Ano1 expression in organotypic cultures of Ano1 WT small intestine.