ライフサイエンスコーパス: calcium entry

1 tore depletion, KSR2 is required for optimal calcium entry.

2 maining adaptation process is independent of calcium entry.

3 appear to depend explicitly on the route of calcium entry.

4 stain calcium signals through store-operated calcium entry.

5 esicles (SVs) that are distal to the site of calcium entry.

6 binding of annexins to membranes at sites of calcium entry.

7 nto signalosomes, resulting in BCR-activated calcium entry.

8 type channels contribute modestly to overall calcium entry.

9 to investigate the mechanism of PACAP-evoked calcium entry.

10 ediated signaling or store depletion-induced calcium entry.

11 4 mM) was added to suppress channel-mediated calcium entry.

12 to synchronous EPSC amplitude, activity, and calcium entry.

13 mechanism (fast adaptation) does not require calcium entry.

14 otide-dependent pathways coupled to neuronal calcium entry.

15 rform other roles unrelated to voltage-gated calcium entry.

16 l Ca(2+), also referred to as store-operated calcium entry.

17 ming that fast adaptation does not depend on calcium entry.

18 zation of T cells using KCl does not lead to calcium entry.

19 coupled to intracellular calcium release and calcium entry.

20 to contribute to action potential-dependent calcium entry.

21 n including decreased chemotaxis and reduced calcium entry.

22 rane calcium influx channels or capacitative calcium entry.

23 showing the critical role of TRPM2-mediated calcium entry.

24 tivates STIM1/Orai1-dependent store-operated calcium entry.

25 ts deficiency had no effect on TCR-initiated calcium entry.

26 release is associated with CaV and not TRPV1 calcium entry.

27 acute loss of Orai1-dependent store-operated calcium entry.

28 stitute the core machinery of store-operated calcium entry.

29 STIM2) are key modulators of store-operated calcium entry.

30 (1) subunit important for excitation-coupled calcium entry?

31 ator (ORAI) pathway controls store-dependent calcium entry, a major mechanism of physiological calciu

32 s as a negative regulator of agonist-induced calcium entry (ACE) that suppresses surface accumulation

33 In eukaryotic cells, calcium entry across the cell surface activates nuclear

34 ular calcium stores activates store-operated calcium entry across the plasma membrane in many cells.

35 sting that the oscillations were mediated by calcium entry across the plasma membrane in response to

36 Calcium entry activated by ablation of both JP45-CASQ1 a

37 During store-operated calcium entry activation, calcium depletion from the end

38 nnels make comparable contributions to total calcium entry after an action potential.

39 ted calcium channels (VGCCs) allow for rapid calcium entry and are expressed during early neural stag

40 y affecting the electrical driving force for calcium entry and calcium channel gating.

41 o pH 6.4 caused inhibition of Orai1-mediated calcium entry and conferred capability for PDGF to evoke

42 ansient receptor potential (TRP)-C1-mediated calcium entry and downstream nuclear factor of activated

43 NA and proteins and abrogated store-operated calcium entry and I(CRAC) in VSMC; control shRNA was tar

44 Global calcium entry and I(SOC) are decreased by S100A6 in a PP

45 sigargin was used to activate store-operated calcium entry and increase cytosolic calcium in endothel

46 r siRNA silencing of P2X(7) receptors blocks calcium entry and inhibits T-cell activation.

47 erpotentials, which often follow APs, affect calcium entry and neurotransmitter release.

48 alcium channels (Cav) are the major route of calcium entry and regulate multiple functions such as co

49 s reveal a more complex relationship between calcium entry and release from stores.

50 findings demonstrate the close apposition of calcium entry and release sites and the dynamics of such

51 Ps), particularly the falling phase, affects calcium entry and small changes in calcium influx can pr

52 per (Slo3) are core regulators of sperm tail calcium entry and sperm hyperactivated motility.

53 In particular, reduced spike height reduces calcium entry and subsequent calcium-activated potassium

54 During inflammation endothelial cell calcium entry and the calcium-related signaling events a

55 This triggers Lyn/Syk-dependent calcium entry and the production of reactive oxygen spec

56 Tonic synapses are specialized for sustained calcium entry and transmitter release, allowing them to

57 1 substantially reduced thapsigargin-induced calcium entry, and more modestly diminished the frequenc

58 idual oligomers larger than trimers inducing calcium entry as they cross the cell membrane, a result

59 is a rare genetic disorder of store-operated calcium entry, associated with a complex syndrome includ

60 Moreover, we show that WAVE2 regulates calcium entry at a point distal to PLCgamma1 activation

61 During irregular firing, calcium entry at both timescales can be detected, sugges

62 e to polyamine-mediated rectification, favor calcium entry at hyperpolarized potentials.

63 nstrate that cholinergic excitation promotes calcium entry at subthreshold membrane potentials to rap

64 This mechanism regulates calcium entry at the end of APs and therefore stabilizes

65 redict human genes involved in mitochondrial calcium entry based on clues from comparative physiology

66 s well as display robust apoptosis following calcium entry blockade.

67 well as display far less apoptosis following calcium entry blockade.

68 ular calcium or inhibition of store-operated calcium entry blocked DIR, but the L-type calcium channe

69 d STIM2 punctum formation and enhanced basal calcium entry but decreased sarco/endoplasmic reticulum

70 MEM20 (POST), does not affect store-operated calcium entry but does reduce plasma membrane Ca(2+) pum

71 llular calcium or inhibition of capacitative calcium entry by 2-APB prevented ciglitazone-induced EGF

72 -1, -2, and -3 enhanced thapsigargin-induced calcium entry by 50-150% in cells stably overexpressing

73 Pharmacological inhibitors of calcium entry, calmodulin activation, and CaMKII activit

74 lates proliferation by inducing capacitative calcium entry (CCE).

75 ed receptor expression was due to attenuated calcium entry, cells were incubated with the calcium che

76 as recently been shown to exhibit myocardial calcium entry channel blocking activity, substantially h

77 Interestingly, the store-operated calcium entry channel inhibitor (SK&F96365) also reduced

78 sing a mouse model in which the gene for the calcium entry channel protein, Orai1, has been deleted.

79 n in stores, and Orai-1, the calcium-induced calcium entry channel, are colocalized with SP, in the s

80 nt receptor potential vanilloid 4 (Trpv4), a calcium-entry channel, is expressed in normal cholangioc

81 ntrolling cell function, can be generated by calcium entry channels activated by plasma membrane depo

82 lcium stores to plasma membrane capacitative calcium entry channels.

83 culum calcium release-induced store-operated calcium entry contributes to intracellular calcium incre

84 f the filtration coefficient, in a dose- and calcium-entry dependent manner.

85 Store-operated calcium entry depicts the movement of extracellular Ca2+

86 ons in the L-type calcium channel that abort calcium entry do not produce this phenotype.

87 re, we reconcile existing data and show that calcium entry does not drive the fastest adaptation proc

88 reas streptomycin antagonized TRPM8-mediated calcium entry, downregulated UCP-1 expression, and mitig

89 ient as CaV2.2 N-type channels at supporting calcium entry during action potential-like stimuli.

90 nd not STIM2 that is exclusively involved in calcium entry during calcium oscillations.

91 te an AHNAK1-dependent mechanism controlling calcium entry during CTL effector function.

92 ads to a complete loss of excitation-coupled calcium entry during KCl depolarization and a more rapid

93 d to the mitochondrial matrix, we found that calcium entry during pacemaking created a basal mitochon

94 ed CPK32 activates CNGC18, further promoting calcium entry during the elevation phase of Ca(2+) oscil

95 The comparison of excitation-coupled calcium entry (ECCE) between FDB fibers from WT, JP45KO,

96 sms of action is to block excitation-coupled calcium entry (ECCE) in both adult mouse flexor digitoru

97 mational coupling, termed excitation-coupled calcium entry (ECCE) is triggered by the alpha(1s)-DHPR

98 ypothesize that under conditions of enhanced calcium entry, elevation of intracellular calcium will r

99 A is required for EGF-induced store-operated calcium entry essential for pancreatic cancer cell migra

100 ize, indicating that a separate mechanism of calcium entry exists, corresponding to cell loss at the

101 In hippocampal pyramidal neurons, calcium entry following an action potential burst result

102 tsynaptic spiking alone and that it requires calcium entry following synaptic NMDA receptor activatio

103 microns away from the wound, allowing direct calcium entry from extracellular fluid into damaged cell

104 craniosensory fibers release glutamate using calcium entry from two sources: CaVs and TRPV1.

105 PLN at the membrane surface proximal to the calcium entry funnel of SERCA.

106 After chemical blockade of Orai1-mediated calcium entry, however, PDGF caused redistribution.

107 esults indicate that the P2Y6/store-operated calcium entry/IL-8 axis is involved in MSU crystal-induc

108 (s) involved in regulation of store operated calcium entry in Darier's disease (DD) is not known.

109 c Cav-1, we show that Cav-1 is essential for calcium entry in endothelial cells and governs the local

110 mbrane potential but abolishes mitochondrial calcium entry in intact and permeabilized cells, and att

111 nnels, thereby inhibiting glucose-stimulated calcium entry in isolated mouse pancreatic beta cells.

112 annel opening, providing a new mechanism for calcium entry in lymphocytes.

113 lcium-selective cation channels that mediate calcium entry in many different cell types.

114 RAC) channels constitutes a primary route of calcium entry in most cells.

115 stnatal development, we quantified EPSCs and calcium entry in MSO neurons of Mongolian gerbils of eit

116 wanted cross-talk between pathways, sites of calcium entry in neurons are localized to specific membr

117 of the proteasome is dependent upon external calcium entry in part through N-methyl-D-aspartate recep

118 pen with fast kinetics and carry substantial calcium entry in response to individual action potential

119 this study, we show that RBCs exhibit robust calcium entry in response to mechanical stretch and that

120 Calcium entry in response to store depletion with thapsi

121 d non-functional Orai1 R91W attenuated basal calcium entry in shTRPC2 cells.

122 ASQ1 (CASQ, calsequestrin) and JP45-CASQ2 on calcium entry in slow twitch muscles.

123 sed on activation of neuronal store-operated calcium entry in spines.

124 n STIM1 completely abolishing store-operated calcium entry in T cells.

125 nificant deficits in BCR triggering-mediated calcium entry in the cytosol, which correlates with impa

126 it caused calcium release and Orai1-mediated calcium entry in the same time period.

127 Thus, Cav-1 is required for calcium entry in vascular endothelial cells and perhaps

128 a(2+) channels (LTCC) are the main route for calcium entry in vascular smooth muscle cells (VSMC).

129 t effect on endogenous, thapsigargin-induced calcium entry in wild-type cells (HEK-293, COS1), in HEK

130 erning why other known routes of significant calcium entry, in particular, VGCCs, are not similarly t

131 and DeltaE9 cells showed larger capacitative calcium entry indicating a direct effect on Ca2+ influx

132 nous TRPC1 or TRPC4 inhibited store-operated calcium entry, indicating they are part of the native SO

133 Activation of alternative routes of calcium entry induced neuronal death in proportion to th

134 and protect the endothelial barrier against calcium entry-induced disruption.

135 Further, calcium entry-induced endothelial barrier disruption is

136 influx, which was blocked by store-operated calcium entry inhibitors.

137 ch recently were suggested to play a role in calcium entry into CD4(+) T cells.

138 Various cellular signals initiate calcium entry into cells, and there is evidence that lip

139 dies described here show that HBx stimulates calcium entry into cells, resulting in an increased plat

140 ve hypothesized that digitoxin might mediate calcium entry into cells.

141 , cell growth, and phospholipase C-dependent calcium entry into cells.

142 Although calcium entry into endothelial cells is critical for los

143 Calcium entry into excitable cells is an important physi

144 report here that digitoxin molecules mediate calcium entry into intact cells.

145 annexins and calcium, resulting in enhanced calcium entry into MV.

146 Calcium entry into myocytes drives contraction of the em

147 epolarization but not after 1 hr and require calcium entry into neurons.

148 gonist-induced hyperactivation and increased calcium entry into platelets.

149 ved as one of the most important players for calcium entry into presynaptic endings responsible for t

150 pecifically, we show that CpG/SR-B1 triggers calcium entry into primary B lymphocytes via phospholipa

151 g-induced synchronization facilitated robust calcium entry into Primed Neurons.

152 uration CS responses in Purkinje cells, more calcium entry into Purkinje cells, larger synaptic depre

153 Synchronous release is tied to calcium entry into synaptic boutons via P/Q type calcium

154 Here we have shown an additional route for calcium entry into T cells-through the low-voltage-activ

155 y, these alterations were found to be due to calcium entry into the mitochondria, because the swellin

156 hondrial calcium uniporter (MCU) facilitates calcium entry into the mitochondrial matrix to stimulate

157 Calcium flux through store-operated calcium entry is a central regulator of intracellular ca

158 Calcium overload due to enhanced calcium entry is a mechanism for spontaneous calcium rel

159 A unique mechanism called store-operated calcium entry is activated when ER calcium is depleted,

160 In support of this, presynaptic calcium entry is affected by afterpotentials after stand

161 hat pairing IP3 with climbing fiber-mediated calcium entry leads to a large calcium release transient

162 e show that the activation of Orai1-mediated calcium entry leads to enhancing focal adhesion turnover

163 onal white noise accelerated the decrease in calcium entry, leaving membrane properties unaffected.

164 f extracellular calcium through capacitative calcium entry may be an unrecognized component that prov

165 We identified a novel plasma membrane calcium entry mechanism that extends the range of rod ph

166 led that caspase-3 activation, extracellular calcium entry, mitochondrial membrane permeability, and

167 th PEMF exposure, attenuated PEMF-stimulated calcium entry, mitochondrial respiration, proliferation,

168 ly demonstrated that neuronal store-operated calcium entry (nSOC) in hippocampal neurons is regulated

169 barrage firing, suggesting that the required calcium entry occurs in other cells.

170 In immune cells, calcium entry occurs through store-operated Ca(2+) relea

171 mGluR-dependent plasticity is independent of calcium entry or calcium dynamics.

172 ivated by depolarization (excitation-coupled calcium entry or ECCE).

173 hat requires store depletion (store-operated calcium entry or SOCE) and a second that is independent

174 In addition to regulating calcium entry, our data suggest that eicosanoid-activate

175 cium channel CaV1.3 constitutes an important calcium entry pathway implicated in the regulation of sp

176 STIM1 activation and did not activate the PM calcium entry pathway.

177 ol-stimulated, or carbachol (CCh)-stimulated calcium entry pathways in HEK-293 cells.

178 al level in the regulation of store-operated calcium entry pathways.

179 on conductance (I(CAN)) that is activated by calcium entry predominantly through L-type calcium chann

180 as a predominant mediator of store-operated calcium entry, proliferation, and cytokine production in

181 Downstream of calcium entry, RCH conditions significantly increased th

182 w that STIM1, an activator of store-operated calcium entry, regulates the dynamics of microtubule-bin

183 in naive CD8(+) T cells, and is critical for calcium entry required for their proper function during

184 posed to form nonselective receptor-operated calcium entry (ROCE) cation channels that are activated

185 d Ca2+ (I(crac)) channels and store-operated calcium entry (SOC) channels.

186 e in cell proliferation rate, store-operated calcium entry (SOCE) amplitude, cationic channel TRPC6,

187 gnaling pathways initiated by store-operated calcium entry (SOCE) are known to regulate neutrophil ac

188 the present study, we report store-operated calcium entry (SOCE) as a novel target of TRPM7 kinase a

189 Our previous studies implied store-operated calcium entry (SOCE) as the major pathway for this Ca(2+

190 Store-operated calcium entry (SOCE) by calcium release activated calciu

191 ers ER morphology and affects store-operated calcium entry (SOCE) by decreasing STIM1 puncta formatio

192 attenuated by inhibiting the store-operated calcium entry (SOCE) channel Orai1.

193 We hypothesized that the store-operated calcium entry (SOCE) channel, Orai1, participates in the

194 sed to form Ca(2+)-selective, store-operated calcium entry (SOCE) channels that are activated by stor

195 allowed a novel "permissive" store-operative calcium entry (SOCE) following the initial platelet-acti

196 model wherein STIM1-mediated store-operated calcium entry (SOCE) governs the Ca(2+) signaling requir

197 ing intracellular calcium and store-operated calcium entry (SOCE) in fast- and slow-twitch muscle fib

198 rine neutrophils show loss of store-operated calcium entry (SOCE) in response to both soluble ligands

199 nnel subunit that facilitates store operated calcium entry (SOCE) in T cells and is necessary for for

200 Store-operated calcium entry (SOCE) is a key evolutionarily conserved p

201 Store-operated calcium entry (SOCE) is a major Ca(2+) signaling pathway

202 Store-operated calcium entry (SOCE) is a ubiquitous mechanism that is m

203 Store-operated calcium entry (SOCE) is an important Ca(2+) entry pathwa

204 Store-operated calcium entry (SOCE) is important in the maintenance of

205 Store-operated calcium entry (SOCE) is involved in various cellular fun

206 Store-operated calcium entry (SOCE) is the mechanism by which extracell

207 Store-operated calcium entry (SOCE) is the predominant Ca(2+) entry mec

208 Store operated calcium entry (SOCE) is thought to primarily regulate ca

209 Transcriptional regulation by Store-operated Calcium Entry (SOCE) is well studied in non-excitable ce

210 By inhibiting store-operated calcium entry (SOCE) or voltage-gated Ca(2+) channels (V

211 uired Ca(2+) flux through the store-operated calcium entry (SOCE) pathway and accompanied plasma memb

212 The store-operated calcium entry (SOCE) pathway is an important route for g

213 Store-Operated Calcium Entry (SOCE) plays key roles in cell proliferati

214 ent advances in understanding store-operated calcium entry (SOCE) regulation, the fundamental questio

215 etion of ER calcium activates store-operated calcium entry (SOCE) through activation of the ER calciu

216 e of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalemmal calcium channe

217 ogical studies suggested that store-operated calcium entry (SOCE), a calcium refilling mechanism resp

218 ntrations in GC cells through store-operated calcium entry (SOCE), and then mediated Ca(2+)-dependent

219 ological characteristics with store-operated calcium entry (SOCE), is required to maintain baseline [

220 ed Ca(2+) signaling, known as store-operated calcium entry (SOCE), occurs downstream of immunorecepto

221 mmune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers

222 amatically inhibited (52-68%) store-operated calcium entry (SOCE), whereas suppression of TRPC4 or TR

223 been considered as a part of store-operated calcium entry (SOCE).

224 the subsequent activation of store-operated calcium entry (SOCE).

225 ochondrial calcium uptake and store-operated calcium entry (SOCE).

226 elated with the occurrence of store-operated calcium entry (SOCE).

227 by calcium store release and store-operated calcium entry (SOCE).

228 melastatin 7 (TRPM7) reduces store-operated calcium entry (SOCE).

229 tion-contraction coupling and store-operated calcium entry (SOCE).

230 lcium influx pathway known as store-operated calcium entry (SOCE).

231 sensor protein that initiates store-operated calcium entry (SOCE).

232 This mechanism is called store-operated calcium entry (SOCE).

233 tified two main components of store-operated calcium entry (SOCE): the endoplasmic reticulum-localize

234 , and indicate that inhibitors of ADPR-gated calcium entry, such as 8Br-ADPR, have the potential to b

235 that exocytosis was more loosely coupled to calcium entry than in fast synapses.

236 olecular mechanism underlying store-operated calcium entry that replenishes ER stores in mouse Muller

237 tions augmented colbalt influx, a marker for calcium entry that selectively occurs through calcium pe

238 ous pacemakers with broad spikes, leading to calcium entry that was weakly buffered.

239 rimary pathway for so-called "store-operated calcium entry" - the cellular entry of calcium induced b

240 Under conditions of enhanced calcium entry, the rate of calcium uptake was faster com

241 that CFTR dysfunction in platelets increased calcium entry though the transient receptor potential ca

242 Calcium entry through a plasma membrane defect leads to

243 by conduction to adjacent SMCs where phasic calcium entry through CavL sums to produce tone.

244 Local calcium entry through CRAC channels activates expression

245 nductances generated by firing revealed that calcium entry through ICAT controls the emergence of the

246 ent with physiological findings showing that calcium entry through L-type calcium channels in pyramid

247 channels causes membrane depolarization and calcium entry through L-type calcium channels.

248 vious work has shown that activity-dependent calcium entry through L-type channels elevates perinucle

249 Activity-dependent calcium entry through L-type channels increased mitochon

250 drugs approved for human use can antagonize calcium entry through L-type channels, these results poi

251 Calcium entry through postsynaptic NMDA-Rs and subsequen

252 In addition, the model shows that calcium entry through store-operated calcium channels is

253 The inhibition is not due to calcium entry through store-operated channels but rather

254 in the sarcoplasmic reticulum, by subsequent calcium entry through store-operated channels, and by in

255 the ductus arteriosus at birth is related to calcium entry through store-operated channels, encoded b

256 Tight regulation of calcium entry through the L-type calcium channel CaV1.2

257 We previously showed in vitro that calcium entry through Trpc1 ion channels regulates myobl

258 re-operated channels but rather results from calcium entry through TRPC7 channels themselves.

259 ion of the TRPM2 pore mutant E960D, in which calcium entry through TRPM2 is abolished, also resulted

260 reases in glutamate release, suggesting that calcium entry through TRPV1 channels may trigger glutama

261 action-potential duration, which would limit calcium entry through voltage-dependent calcium channels

262 Calcium entry through voltage-gated calcium channels has

263 ls is critical for calcium oscillations, but calcium entry through voltage-gated channels has much le

264 The CNGC-mediated calcium entry thus provides a critical link between the

265 ntaining receptors on syntaxin-1 opening and calcium entry to enhance probability of vesicle fusion.

266 rapidly due to lipid peroxidation, allowing calcium entry to initiate lysosome fusion.

267 of neurotransmitters and drugs that inhibit calcium entry, transmitter release and nociception throu

268 xygenation status resulting in extracellular calcium entry, uncouples RGS9-2 from R7BP, triggering it

269 were hyperproliferative and showed enhanced calcium entry upon T cell receptor stimulation.

270 ents, as a tool to investigate mechanisms of calcium entry upon wounding.

271 lly-uncoupled canine wedge model of enhanced calcium entry, using I(Ks) blockade with beta-adrenergic

272 maintain [Ca(2+)]i at extremely low levels; calcium entry usually occurs briefly, and within seconds

273 excitable cells are profoundly influenced by calcium entry via both store-operated and store-independ

274 to ER-plasma membrane junctions, leading to calcium entry via Ca(2+) release-activated Ca(2+) (CRAC)

275 These data suggest that during hypoxia, calcium entry via CRAC channels leads to AMPK activation

276 s expressing C4958S- or C4961S-RyR1 triggers calcium entry via ECCE that resembles that for wild-type

277 ients induced by tetanic stimulation rely on calcium entry via La(3+)- and nifedipine-sensitive calci

278 These results suggest that calcium entry via Orai1 is the predominant SOCE that coo

279 ement of T cell receptors (TCRs) followed by calcium entry via store-operated calcium channels.

280 s well as thapsigargin, a known activator of calcium entry via store-operated channels, all increased

281 ansmission depends critically on presynaptic calcium entry via voltage-gated calcium (Ca(V)) channels

282 how that burst-induced depression depends on calcium entry via voltage-gated channels, is blocked by

283 Store-operated calcium entry was also reduced in peripheral blood monon

284 In TRPC1-KD cells, receptor-operated calcium entry was decreased.

285 Basal calcium entry was enhanced in shTRPC2 cells, whereas the

286 Finally, calcium entry was found to be dependent upon generation

287 lcium-replenishing process of store-operated calcium entry was impaired in MFN2 knockdown cells, wher

288 Store-operated calcium entry was indistinguishable between the two cell

289 Calcium entry was significantly reduced when Orai1 funct

290 selective blockers indicated that the lethal calcium entry was via reverse operation of a sodium-calc

291 es calcium-dependent inactivation and limits calcium entry, whereas CaBP1 blocks calcium-dependent in

292 affecting the cytoskeleton near the site of calcium entry, whereas calcium-dependent dendritic growt

293 ude, and shape of the AP falling phase alter calcium entry, which can affect neurotransmitter release

294 plex to displace synaptotagmin downstream of calcium entry, which has been demonstrated to be importa

295 Here we show that TRPV6 mediates calcium entry, which is highly increased in PCa due to t

296 Calcium entry, which is initially facilitated by transie

297 rs through a process known as store-operated calcium entry, which is initiated by calcium sensor prot

298 ation of the uterine smooth muscle cells and calcium entry, which may contribute to uterine contracti

299 asmic reticulum (ER) induced large sustained calcium entry, which was blocked by SOC inhibitors, but

300 subunits, and observe the diffusive wave of calcium entry within the dendritic spine that follows ch