ライフサイエンスコーパス: CRAC channel

1 ing a single Na(+) ion along the pore of the CRAC channel.

2 oxidant stress and Ca(2+) signaling via the CRAC channel.

3 ores, whereas ORAI1 is a pore subunit of the CRAC channel.

4 to the N and C termini of Orai1 to open the CRAC channel.

5 in the mitochondria to Ca(2+) influx by the CRAC channel.

6 ncluding the functional stoichiometry of the CRAC channel.

7 Ca(2+) signaling by Ca(2+) microdomains near CRAC channels.

8 s necrosis were almost abolished by blocking CRAC channels.

9 ty and gating are mechanistically coupled in CRAC channels.

10 ally advanced the molecular understanding of CRAC channels.

11 feedback relationship exists between RyR and CRAC channels.

12 derstand the unique permeation properties of CRAC channels.

13 ith biophysical properties distinct from the CRAC channels.

14 by a marked increase in Ca2+ influx through CRAC channels.

15 age-gated L-type (Cav1.2) and store-operated CRAC channels.

16 interact with ORAI1, the pore subunit of the CRAC channels.

17 rding, these fusions are fully functional as CRAC channels.

18 nhibits the ability of STIM1 to activate the CRAC channels.

19 is capable of regulating store-operated non-CRAC channels.

20 ompanies the opening of store-operated Orai1/CRAC channels.

21 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channel.

22 unit of the Ca(2+) release-activated Ca(2+) (CRAC) channel.

23 unit of the Ca(2+) release-activated Ca(2+) (CRAC) channel.

24 ulation are Ca(2+) release-activated Ca(2+) (CRAC) channels.

25 re-operated Ca(2+)-release-activated Ca(2+) (CRAC) channels.

26 blockers of Ca(2+) release-activated Ca(2+) (CRAC) channels.

27 (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels.

28 mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels.

29 -membrane calcium-release activated calcium (CRAC) channels.

30 mponents of Ca(2+) release-activated Ca(2+) (CRAC) channels.

31 -operated calcium-release-activated calcium (CRAC) channels.

32 try through Ca(2+) release-activated Ca(2+) (CRAC) channels.

33 achinery of Ca(2+) release-activated Ca(2+) (CRAC) channels.

34 m entry via Ca(2+) release-activated Ca(2+) (CRAC) channels.

35 pening of calcium release-activated calcium (CRAC) channels.

36 -operated calcium release-activated calcium (CRAC) channels.

37 ent (Ip) on Ca(2+) release-activated Ca(2+) (CRAC) channels.

38 try through Ca(2+) release-activated Ca(2+) (CRAC) channels.

39 els are the Ca(2+) release-activated Ca(2+) (CRAC) channels.

40 mark of the Ca(2+) release-activated Ca(2+) (CRAC) channel, a prototypic store-operated Ca(2+) channe

41 it of the calcium release-activated calcium (CRAC) channel, a store-operated channel that is central

42 gonistic and antagonistic modes of action on CRAC channels, acting at the channel level as a store-in

43 Local calcium entry through CRAC channels activates expression of c-fos- and nuclear

44 positively charged sequence of STIM1 in its CRAC channel activating domain, human residues 384-386,

45 among [Ca(2+)](ER), STIM1 redistribution and CRAC channel activation and identify STIM1 oligomerizati

46 expressing an ER-targeted Ca(2+) indicator, CRAC channel activation and STIM1 redistribution follow

47 ensor STIM1 and the channel subunit Orai1 in CRAC channel activation are becoming well understood, th

48 We find that gene expression following CRAC channel activation is an all-or-nothing event over

49 CRAC channel activation occurs, at least in part, throug

50 e cellular and molecular choreography of the CRAC channel activation process, and it is now establish

51 -APB may reflect a store-independent mode of CRAC channel activation that opens a relatively nonselec

52 epletion of this calcium store that triggers CRAC channel activation, it is the pool of STIM1 constit

53 nce of increased [AMP] through ROS-dependent CRAC channel activation, leading to increases in cytosol

54 e preconditions of the unique fingerprint of CRAC channel activation, provide a valuable source for f

55 STIM1 and Orai1 in T cells, as essential for CRAC channel activation.

56 molecular mechanism of channel gating by the CRAC channel activator, stromal interaction molecule 1 (

57 Orai and STIM proteins in the regulation of CRAC channel activity and other non-CRAC channel-related

58 e of these molecules, compound 5D, inhibited CRAC channel activity by blocking ion permeation.

59 Restoring authentic CRAC channel activity required both the presence of STIM

60 ately 2 STIM1:Orai1, suggesting that maximal CRAC channel activity requires binding of eight STIM1s t

61 tosolic Ca(2+) , are important regulators of CRAC channel activity under physiological conditions of

62 cells, large amplitude Ca(2+) oscillations, CRAC channel activity, and downstream Ca(2+)-dependent n

63 he endoplasmic reticulum membrane regulating CRAC channel activity, whilst the minor pool of plasma m

64 novel class of small molecules that inhibit CRAC channel activity.

65 ai1 complex through TRPC1epsilon suppressing CRAC channel activity.

66 annel gating, thereby establishing authentic CRAC channel activity.

67 , that together form the molecular basis for CRAC channel activity.

68 can be independently modulated to fine-tune CRAC channel activity.

69 ering, mitochondrial Ca(2+) uptake regulates CRAC channel activity.

70 i1 are altered by two powerful modulators of CRAC channel activity: extracellular Ca(2+) and 2-APB.

71 constitutively active, conformation for the CRAC channels actually prevent activation of the ARC cha

72 Similarly, maximal activation of endogenous CRAC channels also fails to affect PLC activity.

73 are the primary components of the neutrophil CRAC channel and identifies subpopulations of neutrophil

74 However, how STIM1 communicates with the CRAC channel and initiates the subsequent events culmina

75 erated Ca(2+)-dependent slow inactivation of CRAC channels and a subsequent loss of excitation-transc

76 tail their ionic currents to those of native CRAC channels and channels generated from monomeric Orai

77 inding and resulted in partial activation of CRAC channels and clustering of STIM1 independently of s

78 e that a positive-feedback cascade involving CRAC channels and cysteinyl leukotrienes constitute a no

79 Here, we review the key pore properties of CRAC channels and discuss recent progress in addressing

80 the cysteinyl leukotriene receptor activated CRAC channels and evoked prominent store-operated Ca(2+)

81 ere, we directly probed the pore diameter of CRAC channels and found that 2-APB enlarged the pore siz

82 rate that enamel cells have SOCE mediated by CRAC channels and implicate them as a mechanism for Ca(2

83 hibited store-operated Ca(2+) influx through CRAC channels and responded to cysteinyl leukotrienes.

84 nal change in Orai1 during the activation of CRAC channels and reveal that STIM1-Orai1 interaction an

85 Orai1 forms the pore subunit of CRAC channels and Stim1 is the endoplasmic reticulum (ER

86 se findings reveal new functional aspects of CRAC channels and suggest that the selectivity filter of

87 cells and enamel organ cells is mediated by CRAC channels and that Ca2+ signals enhance the expressi

88 ls have been identified - the store-operated CRAC channels and the store-independent arachidonic acid

89 the store-operated Ca(2+) release-activated CRAC channels and the store-independent arachidonic acid

90 Although both the calcium store-dependent CRAC channels and the store-independent ARC channels are

91 re of the calcium release-activated calcium (CRAC) channel and generates sustained cytosolic calcium

92 x through calcium release-activated calcium (CRAC) channels and the formation of a stable immunologic

93 ement opens Ca(2+) release-activated Ca(2+) (CRAC) channels and triggers formation of an immune synap

94 with Orai1, the pore-forming subunit of the CRAC channel, and I-mfa is recruited to the TRPC1epsilon

95 r knowledge of the molecular function of the CRAC channel, and suggest new therapies aiming at attenu

96 Orai1 is a pore subunit of CRAC channels, and STIM1 acts as an endoplasmic reticulu

97 ter jointly determine the amplitude of Ip on CRAC channels, and the generation of Ip requires the ope

98 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels, and the store-independent, arachidonic a

99 CRAC channels are a very well-characterized example of s

100 identified as critical for the activation of CRAC channels are also key for activation of the ARC cha

101 CRAC channels are an attractive therapeutic target for a

102 CRAC channels are distinguished by a very high Ca(2+) se

103 CRAC channels are formed by members of the recently disc

104 CRAC channels are formed by ORAI1 proteins in the plasma

105 2+) release-activated Ca(2+) (CRAC) channel; CRAC channels are formed by tetramers of the plasma memb

106 CRAC channels are hexamers of ORAI proteins that form th

107 xpression and proliferation, indicating that CRAC channels are important regulators of mammalian neur

108 channels are regulated by the protein STIM1, CRAC channels are regulated by STIM1 in the endoplasmic

109 CRAC channels are required for the differentiation and f

110 These findings indicate that CRAC channels are the primary mechanism for Ca(2+) influ

111 CRAC channels are tightly linked to expression of the tr

112 Ca(2+)-release-activated Ca(2+) (CRAC) channels are a subtype of SOC channels that are ex

113 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels are a widespread mechanism for generating

114 Ca(2+) release-activated Ca(2+) (CRAC) channels are activated through a mechanism wherein

115 These findings highlight a key role for CRAC channels as regulators of allergen induced inflamma

116 These results reveal a central role for CRAC channels as regulators of astrocyte Ca(2+) signalin

117 s is sufficient to immobilize the tetrameric CRAC channel at ER-PM junctions.

118 fundamental issue of how STIM1 activates the CRAC channel at these sites is unresolved.

119 n understanding the physiological aspects of CRAC channels at an organism level using transgenic anim

120 rives the accumulation and the activation of CRAC channels at ER-PM junctions.

121 The CRAC channel blocker developed by GlaxoSmithKline, GSK-7

122 In cells pre-treated with the CRAC channel blocker Synta-66 Ca(2+) entry was significa

123 nt in Th17 differentiation by treatment with CRAC channel blocker was recapitulated in Orai1-deficien

124 -molecule calcium release-activated calcium (CRAC) channel blocker administered after insult, halted

125 These results suggest that CRAC channel blockers can be considered as chemical temp

126 In vivo administration of CRAC channel blockers effectively reduced the severity o

127 selectivity is not an intrinsic property of CRAC channels but rather a tuneable feature that is best

128 ORAI1 does not make a constitutively active CRAC channel, but suppresses the slow Ca(2+)-dependent i

129 Purified CAD forms a tetramer that clusters CRAC channels, but analysis of STIM1 mutants reveals tha

130 the positive and negative modulation of the CRAC channel by TRPC1epsilon and I-mfa, respectively, fi

131 nt manner, suggesting that 2-APB facilitates CRAC channels by altering the pore architecture.

132 Activation of CRAC channels by store depletion involves the redistribu

133 tively, for Ca(2+)-release activated Ca(2+) (CRAC) channels, channels underlying store-operated Ca(2+

134 unsuspected molecular re-arrangement within CRAC channel clusters is necessary for SOCE.

135 ecular steps enabling activation of SOCE via CRAC channel clusters remain incompletely defined.

136 with and clusters Orai1 hexamers to form the CRAC channel complex.

137 In patients, loss-of-function mutations in CRAC channel components ORAI1 and STIM1 abolish SOCE and

138 ymphocytes, Ca(2+) release-activated Ca(2+) (CRAC) channels composed of Orai1 subunits trigger Ag-ind

139 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels, comprised of STIM1 and Orai1 proteins.

140 CRAC channels consisting of four pore-forming Orai1 subu

141 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels constitute a major pathway for Ca(2+) inf

142 Ca(2+) release-activated Ca(2+) (CRAC) channels constitute the major Ca(2+) entry pathway

143 (SOCE) by calcium release activated calcium (CRAC) channels constitutes a primary route of calcium en

144 pecialized Ca(2+) release-activated calcium (CRAC) channels constitutes the major pathway of intracel

145 This review examines new insights into how CRAC channels control T cell-mediated immunity.

146 ated by the Ca(2+) release-activated Ca(2+) (CRAC) channel; CRAC channels are formed by tetramers of

147 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channel crucial for life.

148 nt subunits results in a graded reduction in CRAC channel currents and that this effect is independen

149 Here we have shown that CRAC channel-deficient patients and mice with ectodermal

150 including PGE2, IL-6, IL-8, and GM-CSF in a CRAC channel-dependent manner.

151 red over the last two decades indicates that CRAC channels display a unique functional pore fingerpri

152 Blocking of CRAC channels drastically decreased recruitment of NFAT

153 ions generated by receptor stimulation or on CRAC channel-driven gene expression.

154 Ca(2+) release-activated Ca(2+) (CRAC) channels elevate cytoplasmic Ca(2+) concentration,

155 lled by the Ca(2+) release-activated Ca(2+) (CRAC) channel encoded by the gene Orai1 that is expresse

156 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels encoded by Orai1 and STIM1 as a major rou

157 tivation of Ca(2+) release-activated Ca(2+) (CRAC) channels encoded by Orai1 and STIM1.

158 e show that Ca(2+) release-activated Ca(2+) (CRAC) channels encoded by stromal interaction molecule 1

159 ation of tyrosine 14 on caveolin-1 regulates CRAC channel-evoked c-fos activation without impacting t

160 Moreover, from a basic science perspective, CRAC channels exhibit a unique biophysical fingerprint c

161 rming subunit of the highly Ca(2+)-selective CRAC channel expressed in hematopoietic cells.

162 The physiological importance of CRAC channels for human health is underscored by studies

163 rtant insights into the in vivo functions of CRAC channels for T cell-mediated immunity.

164 lux through Ca(2+) release-activated Ca(2+) (CRAC) channels formed by ORAI proteins.

165 influx via Ca(2+) release-activated Ca(2+) (CRAC) channels formed by STIM and ORAI proteins is requi

166 s in the human ORAI1 and STIM1 genes abolish CRAC channel function and SOCE in a variety of non-excit

167 ntributions of individual ORAI homologues to CRAC channel function are not well understood.

168 We evaluated the requirement of CRAC channel function for lymphocyte homing using expres

169 Expression of Orai1-E106A inhibited CRAC channel function in human and mouse T cells, and pr

170 the equivalent ORAI1-R91W mutation abolishes CRAC channel function in human T cells resulting in seve

171 Furthermore, inhibition of CRAC channel function in rat lungs prevented the impairm

172 recent breakthrough in our understanding of CRAC channel function is the identification of stromal i

173 we provide evidence that the suppression of CRAC channel function may dampen the increased T cell re

174 er, our data indicate that STIM1, STIM2, and CRAC channel function play distinct but synergistic role

175 ely impaired store-operated Ca(2+) entry and CRAC channel function resulting in a strongly reduced ex

176 phobic gating mechanism has implications for CRAC channel function, pharmacology and disease-causing

177 (STIM) and ORAI, two essential regulators of CRAC channel function.

178 romeric channels with ORAI1 and to attenuate CRAC channel function.

179 d native CRAC channels, we conclude that the CRAC channel functions as a hexamer of Orai1 subunits.

180 1 also explains the dynamic coupling between CRAC channel gating and ion selectivity.

181 he conformational and structural dynamics of CRAC channel gating.

182 CRAC channels generate Ca(2+) signals critical for the a

183 Ca(2+)-release-activated Ca(2+) (CRAC) channels generate sustained Ca(2+) signals that ar

184 ored by studies indicating that mutations in CRAC channel genes produce a spectrum of devastating dis

185 As patients with mutations in the CRAC channel genes STIM1 and ORAI1 show abnormal enamel

186 utations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 and STIM1 abolish store-operat

187 t together with STIM1 maintained the typical CRAC channel hallmarks were distinct from those that con

188 all of which displayed a loss of the typical CRAC channel hallmarks.

189 e key initiation point for activation of the CRAC channels has no effect on ARC channel activity.

190 Local Ca(2+) near CRAC channels has to rise above a threshold level to dri

191 , ORAI2, and ORAI3 are known to comprise the CRAC channel; however, the contributions of individual i

192 4W results in constitutive activation of the CRAC channel in vitro, and spontaneous bleeding accompan

193 Our findings establish a critical role of CRAC channels in controlling lineage identity and effect

194 The opening of CRAC channels in response to depletion of intracellular

195 -Syt2 (E-Syt2S), contribute to activation of CRAC channels in T cells.

196 -independent role of E-Syts in activation of CRAC channels in T cells.

197 nds to Orai1, trapping and activating mobile CRAC channels in the overlying PM.

198 wer; Ca(2+) microdomains near store-operated CRAC channels in the plasma membrane and inositol trisph

199 provides a concise discussion of the role of CRAC channels in these lymphocyte populations and the re

200 lecule 1 (STIM1), an ER Ca(2+) sensor gating CRAC channels, in HEK293 cells revealed that RyR are co-

201 trates that ORAI1 and ORAI2 form heteromeric CRAC channels, in which ORAI2 fine-tunes the magnitude o

202 acilitating SOCE by reducing store-dependent CRAC channel inactivation.

203 1 and the N terminus of Orai1 to evoke rapid CRAC channel inactivation.

204 played the biophysical fingerprint of native CRAC channels, including the distinguishing characterist

205 Activation of CRAC channels induces the production of several key infl

206 With CRAC channels inhibited, the high-affinity form of LFA-1

207 nd DCs, which has important implications for CRAC channel inhibition as a therapeutic strategy to sup

208 In human CD4(+) T cells, CRAC channel inhibition reduced the expression of IL-17A

209 treatment of wild-type mice with a selective CRAC channel inhibitor after EAE onset ameliorated disea

210 ct is reversed when cells are treated with a CRAC channel inhibitor.

211 SOCE in NPCs was blocked by the CRAC channel inhibitors La(3+), BTP2, and 2-APB and West

212 duced apoptosis, suggesting that associating CRAC channel inhibitors or hypocalcemic agents with ritu

213 CRAC channel inhibitors, which have been shown to protec

214 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels initiates key functions such as gene expr

215 d suggest that the selectivity filter of the CRAC channel is a dynamic structure whose conformation a

216 s the activation mechanism for the wild-type CRAC channel is likely regulated by the number of pore w

217 The redistribution of CRAC channels is driven through direct STIM1-Orai1 bindi

218 onstrate that Ca2+ influx via store-operated CRAC channels is essential for CaCC activation, chloride

219 s, and it is now established that opening of CRAC channels is governed through direct interactions be

220 ndicate that exquisite Ca(2+) selectivity in CRAC channels is not hardwired into Orai proteins, but i

221 One of the fundamental properties of CRAC channels is their Ca(2+)-dependent fast inactivatio

222 ondrial Ca(2+) transporter(s) that regulates CRAC channels is unclear and could involve the 40 kDa mi

223 The Ca(2+)-release-activated Ca(2+) (CRAC) channel is responsible for Ca(2+) influx and refil

224 CE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is critical for lymphocyte function and i

225 try through Ca(2+) release-activated Ca(2+) (CRAC) channels is crucial in activating the Ca(2+)-sensi

226 CE) through Ca(2+) release-activated Ca(2+) (CRAC) channels is essential for immunity to infection.

227 that activation of the ARC channels, but not CRAC channels, is uniquely dependent on phosphorylation

228 unit of a calcium release-activated calcium (CRAC) channel, is used as the starting point for molecul

229 mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels, is essential for T cell activation and t

230 ggest that during hypoxia, calcium entry via CRAC channels leads to AMPK activation, Na,K-ATPase down

231 tivation of Ca(2+) release-activated Ca(2+) (CRAC) channels leads to sustained elevation of cytoplasm

232 nter, creating a self-organizing process for CRAC channel localization.

233 rimary human T cells, the RyR are coupled to CRAC channel machinery such that SOCE activates RyR via

234 CE) through Ca(2+) release-activated Ca(2+) (CRAC) channels mediated by STIM and ORAI proteins is a f

235 These results establish a requirement for CRAC channel-mediated Ca(2+) influx for T cell homing to

236 vity of the Ca(2+) release-activated Ca(2+) (CRAC) channel, mediating store-operated currents.

237 enamel mineralization, we hypothesized that CRAC channels might be an important Ca(2+) uptake mechan

238 ization by measuring single T cell levels of CRAC channel modulation, non-translational motility, and

239 d Ca2+ entry (SOCE), and patients with these CRAC channel mutations suffer from anhidrosis and hypert

240 ts demonstrate that STIM1-mediated gating of CRAC channels occurs through an unusual mechanism in whi

241 rai1, supporting the idea that activation of CRAC channels occurs through physical interactions with

242 lcium pump rates and the current through the CRAC channels on ERK1/2 activation dynamics, highlightin

243 ORAI1 accumulates in the plasma membrane and CRAC channels open.

244 nvestigate the gating mechanism of the human CRAC channel Orai1 by its activator, stromal interacting

245 namel cells, we found that key components of CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were e

246 e-localized Ca(2+) release-activated Ca(2+) (CRAC) channel, Orai1, in response to emptying of ER Ca(2

247 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels plays a central role in activation of a r

248 oration of R91W mutant Orai1 subunits in the CRAC channel pore affects the overall magnitude of its c

249 ve recently demonstrated that the functional CRAC channel pore is composed of a tetrameric assembly o

250 we recently demonstrated that the functional CRAC channel pore is formed by a homotetrameric assembly

251 ing a structural framework for understanding CRAC channel pore properties.

252 tics, we introduced cysteine residues in the CRAC channel pore subunit, Orai1, and probed their acces

253 Loss-of-function mutations in the CRAC channel pore-forming protein ORAI1 or the Ca(2+) se

254 epletion, the ER Ca(2+) sensor STIM1 and the CRAC channel protein Orai1 redistribute to ER-plasma mem

255 reticulum (ER) Ca(2+) sensor, and Orai1, the CRAC channel protein, at overlapping sites in the ER and

256 s of the STIM1 gating mechanism in the human CRAC channel protein, ORAI1, and identify V102, a residu

257 M1) and the Ca(2+) release-activated Ca(2+) (CRAC) channel protein Orai1.

258 blots revealed the presence of the canonical CRAC channel proteins STIM1 and Orai1.

259 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channel regulates critical cellular functions, inc

260 ctively, fine-tunes the dynamic range of the CRAC channel regulating osteoclastogenesis.

261 the functional and structural mechanisms of CRAC channel regulation, focusing on recent advances in

262 ation of CRAC channel activity and other non-CRAC channel-related functions.

263 Ca(2+) release-activated Ca(2+) (CRAC) channels represent one main Ca(2+) entry pathway i

264 ting subunit and the pore-forming subunit of CRAC channels, respectively, abolishes this histamine-ev

265 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels, resulting in a form of hereditary severe

266 lasmalemmal Ca(2+) release-activated Ca(2+) (CRAC) channels, RyR blockers reduced the Ca(2+) leak fro

267 These findings show that CRAC channels serve as a major route of Ca(2+) entry in

268 g of the phenotypic spectrum of dysregulated CRAC channel signaling, advance our knowledge of the mol

269 nature of interactions between STIM1 and the CRAC channels, STIM1 in the plasma membrane appears to b

270 ter, we showed that the opening of astrocyte CRAC channels stimulated vesicular exocytosis to mediate

271 We assessed CRAC channel stoichiometry by expressing hexameric conca

272 Initial experiments with the three CRAC channel subtypes CRACM1, CRACM2 and CRACM3 have ind

273 -plasma membrane (ER-PM) junctions where the CRAC channel subunit ORAI1 accumulates in the plasma mem

274 rrents in cells co-expressing STIM1 with the CRAC channel subunit, Orai1, with similar potency.

275 ripheral sites where it co-clusters with the CRAC channel subunit, Orai1.

276 hermore, overexpression of dominant-negative CRAC channel subunits inhibits while co-expression of bo

277 to the B lymphoma cell type, suggesting that CRAC-channel targeting is likely to be more efficient th

278 ations at V102 produce constitutively active CRAC channels that are open even in the absence of STIM1

279 mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels that are activated by stromal interaction

280 mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels that are formed by ORAI1 and its homologu

281 subunit of Ca(2+) release-activated Ca(2+) (CRAC) channels that stimulate downstream signaling pathw

282 Although the molecular components of CRAC channels, the Orai1 pore-forming subunit and the ST

283 by SOCE and the Ca2+ release-activated Ca2+ (CRAC) channel, the prototypical SOCE channel.

284 re-operated Ca(2+) release-activated Ca(2+) (CRAC) channels, the molecular mechanism of channel gatin

285 he role of oscillations might be to activate CRAC channels, thereby ensuring the generation of spatia

286 he slow Ca(2+)-dependent inactivation of the CRAC channel, thus also functioning as a gain-of-functio

287 etermine the stoichiometric requirements for CRAC channel trapping and activation, we expressed mCher

288 mpanying Ca(2+) entry through store-operated CRAC channels triggered gene expression.

289 ent demonstrating that mitochondria regulate CRAC channels under physiological conditions by bufferin

290 and not Na(+) -dependent transport, regulate CRAC channels under physiological conditions.

291 Ca(2+)-release-activated Ca(2+) (CRAC) channels underlie sustained Ca(2+) signalling in l

292 of the hexameric Orai1 concatemer and native CRAC channels, we conclude that the CRAC channel functio

293 In isolated mouse pancreatic acinar cells, CRAC channels were activated by blocking Ca(2+) ATPase p

294 In contrast to the CRAC channels, where the channel pore is composed of onl

295 7 cell function is particularly dependent on CRAC channels, which could be exploited as a therapeutic

296 unit of the Ca(2+) release-activated Ca(2+) (CRAC) channel, which is responsible for store-operated C

297 CE) via the Ca(2+) release activated Ca(2+) (CRAC) channels, which are composed of the plasma membran

298 ctance properties consistent with endogenous CRAC channels, whilst the hexameric construct forms an e

299 the low-conductance, highly Ca(2+)-selective CRAC channels whose activation is dependent on depletion

300 o accumulate at ER-PM junctions and activate CRAC channels without depleting Ca(2+) from the ER.