ライフサイエンスコーパス: store depletion

1 rs to ER-plasma membrane junctions following store depletion.

2 sufficient to generate CRAC current without store depletion.

3 ctrostatic interactions and on the extent of store depletion.

4 le SOCE channel activated by STIM1 following store depletion.

5 tivated by endoplasmic reticulum (ER) Ca(2+) store depletion.

6 of SOC channel in response to internal Ca2+ store depletion.

7 r, Orai1, form a productive interaction upon store depletion.

8 tes into punctae at the cell periphery after store depletion.

9 TIM1 forms oligomers within 5 s after Ca(2+) store depletion.

10 nd in less than a second after initiation of store depletion.

11 tion into puncta at the cell periphery after store depletion.

12 of these ER-PM contacts form in response to store depletion.

13 r treatment with thapsigargin to induce Ca2+ store depletion.

14 whose activation is entirely independent of store depletion.

15 (2+) (CRAC) channels in Jurkat T cells after store depletion.

16 channels in the surface membrane after Ca2+ store depletion.

17 igargin-induced endoplasmic reticulum Ca(2+) store depletion.

18 sated sarcoplasmic reticulum calcium leak or store depletion.

19 ,15-epoxyeicosatrienoic acid, independent of store depletion.

20 for the loss of the permeability response to store depletion.

21 ive store-operated Ca2+ channels (SOC) after store depletion.

22 Ca entry) but also by thapsigargin triggered store depletion.

23 puncta, and this mutant failed to respond to store depletion.

24 hetic diacylglycerols, independently of Ca2+ store depletion.

25 efined the channels activated in response to store depletion.

26 tivating factor-mediated SOCE despite normal store depletion.

27 tained currents that depended on the mode of store depletion.

28 trigger augmented Ca2+ entry following Ca2+ store depletion.

29 calcium entry due to receptor activation or store depletion.

30 enhanced CCE measured by Sr(2+) entry after store depletion.

31 4), which induced endoplasmic reticulum (ER) store depletion.

32 differing degrees of linkage to prior Ca(2+) store depletion.

33 ransients by ryanodine was not simply due to store depletion.

34 lines and does not appear to be activated by store depletion.

35 lent cation entry after thapsigargin-induced store depletion.

36 a Ca2+-selective current activated upon Ca2+ store depletion.

37 ation of phospholipase C and internal Ca(2+) store depletion.

38 rent with similar properties is activated by store depletion.

39 which in intact SMC are activated by Ca(2+) store depletion.

40 l activation of CCE did not require complete store depletion.

41 human platelets that is independent of Ca2+ store depletion.

42 respond to variable degrees of intracellular store depletion.

43 turation, SOCE can no longer be activated by store depletion.

44 d Ca2+ currents were not activated following store depletion.

45 -coupled receptors but independent of Ca(2+) store depletion.

46 phate (IP3) formation and initiation of Ca2+ store depletion.

47 tores membrane are rate limiting for passive store depletion.

48 G protein-coupled receptor activation and/or store depletion.

49 lish coupling of Ca2+ entry channels to Ca2+ store depletion.

50 ted Btk-dependent IP3 production and calcium store depletion.

51 activation of phospholipase C but not after store depletion.

52 th endogenous proteins that are sensitive to store depletion.

53 ng by regulating peak IP3 levels and calcium store depletion.

54 C, by inositol 1,4, 5-trisphosphate, and/or store depletion.

55 d forms STIM/ORAI/AMN complexes after Ca(2+) store depletion.

56 cells, they do so dependent on the level of store depletion.

57 ange of agonist concentrations and levels of store depletion.

58 d full activation of Orai1 in the absence of store depletion.

59 with STIM1-mediated signals induced by full store depletion.

60 alized with STIM1 in the puncta formed after store depletion.

61 Cs also suppressed Ca(2+) entry secondary to store depletion.

62 ic reticulum (ER) Ca(2+) sensor that detects store depletion.

63 to a dramatic increase in Ca(2+) entry after store depletion.

64 lity to generate a large Ca(2+) influx after store depletion.

65 inery that generates the Ca(2+) influx after store depletion.

66 els and clustering of STIM1 independently of store depletion.

67 with STIM1, was activated normally by Ca(2+)-store depletion.

68 sor STIM1, which activates SOCs following ER store depletion.

69 upregulation of SOCE after SNL is driven by store depletion.

70 e STIM1:Orai1 ratio at ER-PM junctions after store depletion.

71 the Ca(2+) gating signal to Orai1 following store depletion.

72 n overall Ca(2+) homeostasis at rest with no store depletion.

73 s where STIM1 puncta are localized following store depletion.

74 ing, which is the physiological stimulus for store depletion.

75 of TRPC1 was increased in cells subjected to store depletion.

76 ting STIM1 movements toward the PM upon Ca2+ store depletion.

77 nt endoplasmic reticulum regions during Ca2+ store depletion.

78 n Ca(2+) entry with or without activation of store depletion.

79 ssociation of TRPC1 from Cav1 in response to store depletion.

80 y phospholipase C-derived messengers or Ca2+ store-depletion.

81 on stemming from its enhanced sensitivity to store-depletion.

82 a 2+ influx triggered by intracellular Ca 2+ stores depletion, a phenomenon known as capacitative Ca

83 oplasmic reticulum Ca(2+) sensors that, upon store depletion, activate Ca(2+) release-activated Ca(2+

84 and proximity ligation assays revealed that store depletion activated STIM1 translocation from withi

85 We conclude that store depletion-activated Ca(2+) entry occurs through ch

86 These cells also possess a Ca(2+) store depletion-activated Ca(2+) entry pathway that is o

87 The data demonstrate that internal Ca2+ store depletion-activated Ca2+ current (ISOC) in this sa

88 rdinately by apamin-sensitive SK current and store depletion-activated Ca2+ current.

89 r the same conditions that reveal endogenous store depletion-activated Ca2+ entry, i.e., classical CC

90 PS1 or PS2 significantly attenuated CCE and store depletion-activated currents.

91 llations in beta-cells is provided by a Ca2+ store depletion-activated nonselective cation current, w

92 2, TRPC4, TRPC5, and TRPC7, can each mediate store-depletion-activated Ca2+ entry in mammalian cells,

93 hese results provide evidence that SR Ca(2+) store depletion activates CCE in parallel with the organ

94 Calcium store depletion activates multiple ion channels, includi

95 n vivo permeation studies revealed that Ca2+ store depletion activates similar nonselective cationic

96 Upon store depletion after T-cell receptor stimulation, STIM1

97 The role of Trp's in Ca2+ entry triggered by store depletion alone is less clear.

98 smic reticulum efficiently counteracts local store depletion and accounts for the spatial spread of C

99 ER) Ca(2+) sensor that responds to ER Ca(2+) store depletion and activates Ca(2+) channels in the pla

100 of TRP channel translocation in response to store depletion and agonist stimulation is not known.

101 ggest that loss of STIM2 may underlie Ca(2+) store depletion and apoptosis resistance in tumor cells.

102 idly activating process which is graded with store depletion and becomes fully activated before compl

103 delimited signaling complex that forms after store depletion and brings calcineurin, via the scaffold

104 ndependently regulated to varying degrees by store depletion and by G protein-coupled receptor activa

105 cells, an impaired biochemical link between store depletion and channel opening is unlikely to be re

106 ical stimuli that do not produce substantial store depletion and depends on interactions among three

107 -endoplasmic reticulum calcium ATPase led to store depletion and dramatic redistribution of STIM1 and

108 It could occur without full Ca2+ store depletion and in less than a second after initiati

109 SOC activity following intracellular calcium store depletion and induction of CCE.

110 II activation following intracellular Ca(2+) store depletion and inhibition of IP3 receptors blocks b

111 or SOCE) and a second that is independent of store depletion and is activated by depolarization (exci

112 is entirely separate from those activated by store depletion and is specifically activated at physiol

113 ulum Ca(2+) sensor that senses intracellular store depletion and migrates to plasma membrane proximal

114 a(2+)-selective channel that is activated by store depletion and regulated by inositol 1,4, 5-trispho

115 1 functions as the missing link between Ca2+ store depletion and SOC influx, serving as a Ca2+ sensor

116 annels, but rather inhibits coupling between store depletion and SOCE activation.

117 These data suggest that both local store depletion and some time-dependent inhibitory mecha

118 A microinjection blocked Ca(2+) influx after store depletion and subsequent Ca(2+) add-back; the Ca(2

119 ion resulted in enhanced Ca(2+) influx after store depletion and subsequent Ca(2+) add-back; the infl

120 s observed between the initiation of calcium store depletion and the activation of Icrac.

121 between Cav1.3-TRPC1-STIM1 was observed upon store depletion and the loss of either TRPC1 or STIM1 le

122 ial cells, and triggers Ca2+ entry following store depletion and the resultant increase in endothelia

123 Store depletion and the subsequent Ca(2+) influx directl

124 CCE activation correlates with the degree of store depletion and the time that is required to refill

125 elusive signaling process senses the Ca(2+) store depletion and triggers the opening of plasma membr

126 f arachidonic acid, complete independence of store depletion, and an absolute requirement for the poo

127 dinium-induced CHOP up-regulation, ER Ca(2+) store depletion, and mitochondrial Ca(2+) accumulation i

128 n the endoplasmic reticulum stress signal of store depletion arises, for example when acidosis inhibi

129 al calcium channels that open in response to store depletion as [Ca(2+)]dts drops.

130 E is that it can also be triggered merely by store depletion, as occurs after inhibition of internal

131 When store depletion becomes widespread, the polymers would c

132 a(2+) entry into rod cytosol is augmented by store depletion, blocked by La(3+) and Gd(3+) and suppre

133 After store depletion, both proteins slow to the same speeds,

134 PM-targeting motif oligomerized after Ca(2+) store depletion but failed to form puncta at ER-PM junct

135 d activation of PKD2 occurs independently of store depletion but requires the activity of phospholipa

136 ease of intracellular Ca2+ secondary to Ca2+ store depletion, but Ca2+ influx induced by these agonis

137 nsible for Ca(2+) influx and refilling after store depletion, but how cells cope with excess Ca(2+) w

138 [Ca2+]i store depletion, but not extracellular Ca2+ chelation, p

139 STIM1 and Orai1 colocalize after store depletion, but Orai1 does not associate detectably

140 ved to initiate oligomerization after Ca(2+) store depletion, but the contributions of STIM1 cytosoli

141 Since store depletion by Ca(2+) ionophore will also activate I

142 Store depletion by thapsigargin also activated this inwa

143 ways show different degrees of dependence on store depletion by thapsigargin and ionomycin, and diffe

144 However, store depletion by thapsigargin is sufficient to activat

145 Here, we show that passive store depletion by thapsigargin or receptor activation b

146 ble to the expression of hTrp3 obtained upon store depletion by thapsigargin was much lower than that

147 yl beta-cyclodextrin had no effect on Ca(2+) store depletion by the G protein-coupled agonists platel

148 Store depletion Ca(2+) entry in both pulmonary and renal

149 dea, human TRPC5 was activated by a standard store-depletion/Ca2+ re-entry protocol, an effect that w

150 their actions on promoting InsP(3)-sensitive store depletion, can be distinguished from Ca(2+)-depend

151 following agonist-induced intracellular Ca2+ store depletion (capacitative Ca2+ entry, CCE) represent

152 eptor activation or by intracellular calcium store depletion [capacitative calcium entry (CCE)].

153 ed in hypothalamic GT1 neuronal cells during store depletion caused by activation of gonadotropin-rel

154 Taken together, store depletion causes activation of voltage-operated Ca

155 Store depletion causes the ER Ca(2+) sensor stromal inte

156 tructure, and stoichiometry was unchanged by store depletion, coexpression with STIM1, or an Orai1 mu

157 solution was changed from control saline to store depletion conditions, and finally to store repleti

158 ical transduction event through which Ca(2+) store depletion controls store-operated Ca(2+) entry, ac

159 hen coexpressed with STIM1 and activated via store depletion, CRACM1 and CRACM2 are facilitated at lo

160 in these cells is completely independent of store depletion, displays a cation selectivity of Ca(2+)

161 Store depletion elicited [Ca(2+)](i) signals that exceed

162 etitive depolarization that does not require store depletion (excitation-coupled Ca(2+) entry, ECCE).

163 ral of these channels are sensors of calcium store depletion, G-protein-coupled receptor activation,

164 ion of store-operated Ca(2+) entry by Ca(2+) store depletion has long been hypothesized to occur via

165 led how STIM1 activates TRPC1 in response to store depletion; however, the role of STIM1 in TRPC chan

166 with protocols that provide extensive Ca(2+) store depletion; however, the role of store-operated ent

167 ternal stores and Ca(2+) influx activated by store depletion (i.e. capacitative or store-operated Ca(

168 If cell-attached patches were formed before store depletion, I(soc) was activated outside but not in

169 he increase in the cytosolic [Ca(2+)] due to store depletion in both pulmonary and renal ASMCs was pr

170 ng cells was required to prevent spontaneous store depletion in calcium-free media.

171 re involved in the ER Ca(2+) refilling after store depletion in ECs.

172 We have reported that internal Ca2+ store depletion in HSY cells stimulates a nonselective c

173 significant extracellular Ca(2+) entry after store depletion in OPCs.

174 Increases in the cytosolic [Ca(2+)] due to store depletion in pulmonary ASMCs required simultaneous

175 fter stimulation with an agonist but also by store depletion in the absence of an agonist.

176 rai1 are activated following internal Ca(2+) store depletion in these cells, it is not clear how the

177 Ca(2+) release-activated Ca(2+) channels via store depletion in VSMC, the pathophysiological agonist

178 ow SOC and I(crac) sense and respond to Ca2+-store depletion: in one model, a messenger molecule is g

179 ted that activates Ca2+ entry in response to store depletion; in an alternative model, InsP3 receptor

180 Thapsigargin-induced store depletion increased lung endothelial permeability

181 We show that store depletion increased partitioning of TRPC1 and STIM

182 trophils (PMNs) and HL60 cells without prior store depletion, independent of G-proteins and of phosph

183 POST-Orai1 binding is store depletion-independent.

184 a-2 signal by 100 microM Mn(2+) following SR store depletion indicated that extracellular Ca(2+) entr

185 Store depletion induced interactions between STIM1 and T

186 and proximity ligation assays revealed that store depletion induced interactions between TRPC1 and G

187 formation required STIM1 expression but not store depletion, induced here by thapsigargin (TG).

188 Store depletion, induced through blockade of sequestrati

189 to study their effect on agonist- as well as store depletion-induced Ca(2+) entry and to test for a r

190 way, to generate cells with constitutive and store depletion-induced Ca(2+) entry.

191 ntial channel (TRPC1), and thereby activates store depletion-induced Ca2+ entry in endothelial cells.

192 y affect fMLP receptor-mediated signaling or store depletion-induced calcium entry.

193 lux in T cells through the inhibition of the store depletion-induced calcium influx.

194 onclude that the adaptive mechanism limiting store depletion-induced endothelial lung injury in the a

195 mechanism for TRPC1 SOCs in VSMCs, in which store depletion induces formation of TRPC1-Galphaq-PLCbe

196 Store depletion induces redistribution of STIM1 into dis

197 Store depletion induces STIM1 to aggregate and relocate

198 ls overexpressing either TRPC3 or TRPC6 in a store-depletion insensitive manner, these TRPCs become s

199 located in the ER lumen and relocalize upon store depletion into puncta closely associated with the

200 Activation of CRAC channels by store depletion involves the redistribution of the ER Ca

201 se to angiotensin II or thapsigargin-induced store depletion is ablated, although the mechanisms are

202 dently of store depletion is tenuous because store depletion is an integral component of the ROCE res

203 ted following T cell receptor (TCR)-mediated store depletion is considered to be a major mechanism fo

204 xact mechanism by which Trp1 is regulated by store depletion is not known.

205 Unexpectedly, Ca(2+) store depletion is not required for activation of Orai1/

206 ological levels of stimulation, where Ca(2+) store depletion is only transient and/or partial, eviden

207 teins, Trp2-mediated Ca2+ entry activated by store depletion is seen under the same conditions that r

208 Orai participating in ROCE independently of store depletion is tenuous because store depletion is an

209 w that although it is dispensable for Ca(2+)-store depletion, KSR2 is required for optimal calcium en

210 ective of whether it is evoked by carbachol, store depletion, lanthanides or elevated intracellular c

211 Ca(2+) store depletion led to a rapid translocation of STIM1 in

212 antitative criterion closely predicts the Ca store depletion level required for spark termination for

213 This was further verified by Ca(2+) store depletion, linking Ca(2+) release to light excitat

214 , suggesting that the initial injury-induced store depletion may be due to increased inositol trispho

215 d by a variety of stimuli, including calcium store depletion, mechanical perturbations, receptor acti

216 identified two proteins required for Ca(2+)-store-depletion-mediated Ca(2+) influx, STIM1 and STIM2.

217 hildren (p < .05), whereas patients with fat stores depletion (midarm fat area 2) had a higher probab

218 Patients at risk for protein stores depletion (midarm muscle areas 1 and 2) had a hig

219 a sensor of Ca(2+) store content that after store depletion moves to the plasma membrane to stimulat

220 Neither I(CRAC) activation by passive store depletion nor the effects of 2-APB were altered by

221 table system for studying the effect of Ca2+-store depletion on SOC and I(crac).

222 puncta." STIM2 translocates into puncta upon store depletion only when coexpressed with STIM1.

223 enerates a sustained Ca(2+) influx through a store depletion-operated pathway and that this drives th

224 ry significant current in response to either store depletion or addition of 2-APB.

225 mplete failure of ECC, independent of Ca(2+) store depletion or block of RyR1 channels.

226 ate the Orai channel without inducing Ca(2+) store depletion or clustering of Orai into punctae yield

227 2+) influx in Orai3-expressing cells without store depletion or co-expression of STIM1.

228 additive tone, which is blunted by internal store depletion or inositol 1,4,5-trisphosphate receptor

229 STIM1 activation by store depletion or mutational modification strongly supp

230 [Ca(2+)](i) elevation evoked by the passive store depletion or TCR ligation.

231 x evoked by thrombin when applied after Ca2+ store depletion, or by activators of PKC.

232 Upon endoplasmic reticulum Ca(2+) store depletion, Orai channels in the plasma membrane ar

233 In the absence of store depletion, plasmalemmal Ca(2+) permeability in res

234 s revealed that agents that enable ER Ca(2+) store depletion promote the development of whole cell in

235 Store depletion promotes STIM1-POST complex binding to s

236 e CRAC channel, colocalizes with STIM1 after store depletion, providing a physical basis for the loca

237 Here, we show that ER Ca(2+)-store depletion rapidly induces STIM1 phosphorylation at

238 The identity of SOCs and their coupling to store depletion remain molecular and mechanistic mysteri

239 Orai3 interacts less well with AKAP79 after store depletion, rendering it ineffective in activating

240 Passive Ca(2+) store depletion resulted in the opening of 41-pS CRAC ch

241 Ca(2+)-store depletion resulted in the rapid entry of external

242 Notably, store depletion results in transient localization of STI

243 Store depletion revealed bimodal Ca(2+) responses to ace

244 gulatory subunits that confer STIM1-mediated store depletion sensitivity to these channels.

245 s exist in skeletal muscle; one activated by store depletion (SOCE) and a second by sustained/repetit

246 following endoplasmic reticulum (ER) Ca(2+) store depletion, specifically due to an increase in extr

247 After Ca(2+) store depletion, STIM1 and Orai couple to each other, al

248 On store depletion, STIM1 lacking all cytosolic domains (ST

249 Upon store-depletion, Stim1 translocates to domains of ER adj

250 Independent of store depletion, STIM2 colocalizes with and blocks the f

251 Ca2+ store depletion stimulates store-operated Ca2+-selective

252 phosphorylation, although it is unclear how store depletion stimulates this gating pathway.

253 active at negative potentials that requires store depletion (store-operated calcium entry or SOCE) a

254 On store depletion, synthetic VSMCs and A7r5 cells display

255 oughout axonal and neurite structures and ER store depletion (thapsigargin) evoked Ca(2+) transients

256 Store depletion that activates TRPC1, via STIM1, inhibit

257 After store depletion, the ER Ca(2+) sensor STIM1 and the CRAC

258 On store depletion, the protein binds STIM1 and moves withi

259 reticulum moves to the plasma membrane upon store depletion thereby enabling inositol 1,4,5-trisphos

260 In addition to Ca(2+) store depletion these SOCs could also be activated by al

261 s in the signaling pathway connecting Ca(2+) store depletion to Ca(2+) influx.

262 the spectrin membrane skeleton couples Ca2+ store depletion to Ca2+ entry.

263 articipates in linking intracellular calcium store depletion to calcium release-activated calcium (CR

264 s a "calcium influx factor," linking calcium store depletion to downstream SOCE.

265 The mechanisms linking store depletion to SOCE remain controversial, hypothetic

266 of the signal coupling intracellular Ca(2+) store depletion to the activation of Ca(2+) entry has lo

267 1), translocates within the ER membrane upon store depletion to the juxtaplasma membrane domain, wher

268 ving as a Ca2+ sensor that translocates upon store depletion to the plasma membrane to activate CRAC

269 l interaction molecule 1 (STIM1) in coupling store depletion to this activation pathway using patch c

270 Surprisingly, the nadir of the store depletion trails the peak of the spark by about 10

271 However, store depletion triggers molecular rearrangements in Ora

272 Since thapsigargin-induced store depletion triggers normal calcium entry in Itk-/-

273 on as a failsafe mechanism to prevent Ca(2+) store depletion under pathophysiological and stress cond

274 tive manner, these TRPCs become sensitive to store depletion upon expression of an exogenous Orai.

275 Ca(2+) store depletion, using ATP (100 microM) or thapsigargin

276 s but inserted into the plasma membrane upon store depletion via a regulated exocytoytic mechanism (v

277 minimal activation of Ca2+ influx by partial store depletion was confirmed by the measurement of Mn2+

278 Surprisingly, Sr(2+) entry in the absence of store depletion was enhanced in BN-treated cells, which

279 nd control oocytes when intracellular Ca(2+) store depletion was induced by microinjection of inosito

280 activation elicited by intracellular calcium store depletion was obviated; 2) EGF-induced CCE fell by

281 h the rate at which the current activates on store depletion was slowed.

282 tly, SOCE after 4-chloro-meta-cresol-induced store depletion was suppressed.

283 nduced by S-nitrosylation and potentiated by store depletion was unaffected by 2-APB, suggesting that

284 phospholipase C-dependent mechanism, not by store depletion, when expressed in HEK293 cells.

285 Channel activation is suggested to depend on store depletion, which redistributes and clusters stroma

286 ivates the same subset of Ca(2+) channels as store depletion, which triggers CCE.

287 ernal medium activated Ca2+ entry after Ca2+ store depletion, which we monitored by changes in cellul

288 After Ca2+ store depletion with caffeine (10 mM), refilling was slo

289 tore-operated Ca(2+) entry (SOCE) by passive store depletion with cyclopiazonic acid, a reversible bl

290 creased Ca2+ influx after intracellular Ca2+ store depletion with either thrombin or thapsigargin.

291 In addition, the rate of Ca2+ store depletion with repetitive local activation of rele

292 itiated by endoplasmic reticulum (ER) Ca(2+) store depletion with subsequent oligomerization of the S

293 2+) was reintroduced, which was amplified by store depletion with thapsigargin (1 mum), and was signi

294 We found that serotonin (5-HT) or store depletion with thapsigargin (TG) enhanced intracel

295 served that the Ca2+ rise elicited following store depletion with thapsigargin is significantly lower

296 Calcium entry in response to store depletion with thapsigargin was reversibly blocked

297 ular Ca(2+) removal and intracellular Ca(2+) store depletion with thapsigargin, inhibited activation

298 hospholipase C-coupled agonist or to calcium store depletion with thapsigargin.

299 entry (SOCE) channels that are activated by store-depletion with Ca(2+) chelators or calcium pump in

300 ediated Ca(2+) oscillations at low levels of store depletion, without interfering with STIM1-mediated