ライフサイエンスコーパス: store depletion

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

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

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

4 nt endoplasmic reticulum regions during Ca2+ store depletion.

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

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

7 ficantly sustain SOCE in response to maximal store depletion.

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

9 sufficient to generate CRAC current without store depletion.

10 ctrostatic interactions and on the extent of store depletion.

11 le SOCE channel activated by STIM1 following store depletion.

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

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

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

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

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

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

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

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

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

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

22 whose activation is entirely independent of store depletion.

23 (2+) (CRAC) channels in Jurkat T cells after store depletion.

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

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

26 sated sarcoplasmic reticulum calcium leak or store depletion.

27 ,15-epoxyeicosatrienoic acid, independent of store depletion.

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

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

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

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

32 hetic diacylglycerols, independently of Ca2+ store depletion.

33 efined the channels activated in response to store depletion.

34 tivating factor-mediated SOCE despite normal store depletion.

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

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

37 calcium entry due to receptor activation or store depletion.

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

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

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

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

42 lent cation entry after thapsigargin-induced store depletion.

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

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

45 rent with similar properties is activated by store depletion.

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

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

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

49 respond to variable degrees of intracellular store depletion.

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

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

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

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

54 tores membrane are rate limiting for passive store depletion.

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

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

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

58 activation of phospholipase C but not after store depletion.

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

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

61 ange of agonist concentrations and levels of store depletion.

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

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

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

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

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

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

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

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

70 els and clustering of STIM1 independently of store depletion.

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

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

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

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

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

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

77 s where STIM1 puncta are localized following store depletion.

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

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

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

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

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

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

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

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

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

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

88 2, TRPC4, TRPC5, and TRPC7, can each mediate store-depletion-activated Ca2+ entry in mammalian cells,

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

90 Calcium store depletion activates multiple ion channels, includi

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

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

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

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

95 Amlodipine as well as approaches that cause store depletion and activate SOCE trigger phosphorylatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 1 functions as the missing link between Ca2+ store depletion and SOC influx, serving as a Ca2+ sensor

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

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

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

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

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

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

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

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

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

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

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

123 cess of sensing and communicating ER calcium-store depletion, and particularly into the STIM1 conform

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

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

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

127 When store depletion becomes widespread, the polymers would c

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

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

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

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

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

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

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

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

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

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

138 ER store depletion by plasma membrane-localized TRPV1 chann

139 Store depletion by thapsigargin also activated this inwa

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

141 However, store depletion by thapsigargin is sufficient to activat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Ca(2+) store depletion destabilized the two EF hands, triggerin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Thapsigargin-induced store depletion increased lung endothelial permeability

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

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

178 RAI activation in a Ca(v)1.2-independent and store depletion-independent manner.

179 POST-Orai1 binding is store depletion-independent.

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

181 Store depletion induced interactions between STIM1 and T

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

183 Store depletion induced interactions between TRPC1 and P

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

185 Store depletion, induced through blockade of sequestrati

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

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

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

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

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

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

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

193 Store depletion induces redistribution of STIM1 into dis

194 Store depletion induces STIM1 to aggregate and relocate

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

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

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

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

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

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

201 These results indicate that rapid store depletion is mediated by Na(+)/Ca(2+) exchange acr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 the Ca(2+)-sensor protein STIM1 upon Ca(2+) store depletion of the endoplasmic reticulum.

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

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

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

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

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

225 2+) influx in Orai3-expressing cells without store depletion or co-expression of STIM1.

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

227 STIM1 activation by store depletion or mutational modification strongly supp

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

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

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

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

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

233 Store depletion promotes STIM1-POST complex binding to s

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

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

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

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

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

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

240 Notably, store depletion results in transient localization of STI

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

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

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

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

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

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

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

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

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

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

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

252 On store depletion, synthetic VSMCs and A7r5 cells display

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

254 Store depletion that activates TRPC1, via STIM1, inhibit

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

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

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

258 active conformation in response to ER Ca(2+) store depletion, thereby interacting with and gating PM-

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

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

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

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

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

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

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

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

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

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

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

270 nteraction molecule 1 (STIM1) in response to store depletion triggered by stimulation of a variety of

271 However, store depletion triggers molecular rearrangements in Ora

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

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

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

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

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

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

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

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

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

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

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

283 ions and phosphorylation of TRPC1 induced by store depletion were both reduced by pharmacological inh

284 Both rapid and slow store depletion were largely unaffected in InsP(3) recep

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

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

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

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

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

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

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

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