ライフサイエンスコーパス: Ca2 entry

1 he store-operated mode of receptor-activated Ca2+ entry.

2 the plasma membrane to allow store-operated Ca2+ entry.

3 ellular calcium and on the driving force for Ca2+ entry.

4 uent stimuli eliciting action potentials and Ca2+ entry.

5 minant suppression of Tg- and OAG-stimulated Ca2+ entry.

6 on of IP3BPs had no effect on store-operated Ca2+ entry.

7 in HEK293 cells modestly enhanced TG-induced Ca2+ entry.

8 el paradigm for feedback control of cellular Ca2+ entry.

9 S2 cells significantly reduced TG-dependent Ca2+ entry.

10 ondary activation of L-type voltage-operated Ca2+ entry.

11 DT40 B-cells, which expresses both forms of Ca2+ entry.

12 roepithelial cells are markedly dependent on Ca2+ entry.

13 , consistent with the coupling hypothesis of Ca2+ entry.

14 ation of L-type channels as the mediators of Ca2+ entry.

15 F96365 two antagonists of agonist-stimulated Ca2+ entry.

16 g acidification that was highly dependent on Ca2+ entry.

17 nt of the permeability response dependent on Ca2+ entry.

18 e GABA synapses, where DA acts by decreasing Ca2+ entry.

19 by regulating the process of store-operated Ca2+ entry.

20 he antibody blocked thrombin- or IP3-induced Ca2+ entry.

21 via a mechanism separate from store-operated Ca2+ entry.

22 sumably via the regulation of store-operated Ca2+ entry.

23 a2+ release, respectively, without affecting Ca2+ entry.

24 el Yvc1 and was independent of extracellular Ca2+ entry.

25 rization) prevented both the association and Ca2+ entry.

26 mportant pathway for synaptically controlled Ca2+ entry.

27 e pathways exist for thapsigargin-stimulated Ca2+ entry.

28 cells exhibited Ca2+ concentration-dependent Ca2+ entry.

29 (Gd3+), partially inhibited hTRPM3-mediated Ca2+ entry.

30 carbachol further augmented hTRPM3-mediated Ca2+ entry.

31 e-sensitive Ca2+ channels and store-operated Ca2+ entry.

32 but this was not associated with subsequent Ca2+ entry.

33 physiological agonist-induced activation of Ca2+ entry.

34 ic reticulum may be fuelled by extracellular Ca2+ entry.

35 through depolarization-induced increases in Ca2+ entry.

36 n mice and was associated with TRPC-mediated Ca2+ entry.

37 nduced TRPC6 knockdown significantly reduced Ca2+ entry.

38 gical inhibition of ICRAC and store-operated Ca2+ entry.

39 family of channels are involved in regulated Ca2+ entry.

40 e when O2 levels fall, causing voltage-gated Ca2+ entry.

41 sm of activation of ICRAC and store-operated Ca2+ entry.

42 We have examined whether store-operated Ca2+ entry, a common pathway for Ca2+ entry in non-excit

43 ecognition of IP3 determines agonist-induced Ca2+ entry (ACE), independent of its Ca2+ release activi

44 ma isoforms are required for agonist-induced Ca2+ entry (ACE).

45 Cs at the onset of beating (day 9) depend on Ca2+ entry across the plasma membrane (50%) whereas Ca2+

46 Phospholipase C signaling stimulates Ca2+ entry across the plasma membrane through multiple m

47 Ca2+ entry activates ERK indirectly, via recruitment of

48 d by mitochondria near plasmalemmal sites of Ca2+ entry acts as a modulator to upregulate the two kin

49 argin added to the external medium activated Ca2+ entry after Ca2+ store depletion, which we monitore

50 that Ca2+ release is the causal trigger for Ca2+ entry after receptor activation.

51 ased (i) Tg- and OAG-stimulated currents and Ca2+ entry and (ii) the level of endogenous TRPC1 but no

52 45Ca2+ was used to study passive Ca2+ entry and active Ca2+ efflux via the plasma membran

53 ding how G-protein-coupled receptors control Ca2+ entry and Ca2+-dependent events such as neurotransm

54 emporal isolation from those events, such as Ca2+ entry and consequent exocytosis, that are normally

55 BK channels or SR Ca2+ uptake, to promoting Ca2+ entry and contractility at term, and relate data on

56 ticotropin leads to depolarization-dependent Ca2+ entry and cortisol secretion.

57 hormonal signals to depolarization-dependent Ca2+ entry and cortisol secretion.

58 ID) syndrome are defective in store-operated Ca2+ entry and CRAC channel function.

59 Antisense TRPC3 similarly reduced Ca2+ entry and endogenous TRPC3.

60 evelopmental changes in the coupling between Ca2+ entry and exocytosis were studied in mouse inner ha

61 Sper1 is essential for depolarization-evoked Ca2+ entry and for hyperactivated movement, a key flagel

62 olarizations Ba2+ entry appeared larger than Ca2+ entry and generated similar but slower pH changes.

63 that in arterial smooth muscle steady-state Ca2+ entry and global [Ca2+]i are regulated by low-activ

64 lowering Stim1 levels reduces store-operated Ca2+ entry and inhibits intestinal epithelial repair aft

65 ther TRPV4 or AQP5 displayed greatly reduced Ca2+ entry and loss of RVD in response to hypotonicity,

66 c reticulum throughout the cell and coupling Ca2+ entry and mitochondrial Ca2+ uptake to Ca2+ release

67 channels are normally vital for presynaptic Ca2+ entry and neurotransmitter release at many central

68 ned to identify regulators of store-operated Ca2+ entry and NFAT nuclear import.

69 ed the involvement of TRPC1 in bFGF-mediated Ca2+ entry and proliferation of embryonic rat neural ste

70 leads to channel inactivation, which limits Ca2+ entry and protects against excitotoxicity.

71 tim as critical components of store-operated Ca2+ entry and showed that dOrai and its human homologue

72 ti-TRPC1 antibody inhibited the VEGF-induced Ca2+ entry and the increased endothelial permeability.

73 Here we show that thrombin-induced Ca2+ entry and the resultant AMP-activated protein kinas

74 fects on mechanisms of both Ca2+ release and Ca2+ entry and the resulting spatial and temporal aspect

75 ization, which reduces the driving force for Ca2+ entry and ultimately causes the potent suppression

76 agonist AR-R17779 while blocking the Na+ or Ca2+ entry and/or inhibiting signaling kinases.

77 endothelial cells augmented the VEGF-induced Ca2+ entry, and application of Ang1 opposed this effect.

78 tore-operated Ca2+ entry (SOC), capacitative Ca2+ entry, and Ca2+ release-activated channel opening (

79 propagation of [Ca2+]c waves, store-operated Ca2+ entry, and mitochondrial Ca2+ uptake, we used two I

80 res or 1-oleoyl-2-acetyl-sn-glycerol-induced Ca2+ entry, and significantly blocks an inward cation cu

81 The cationic current, Ca2+ entry, and transendothelial electrical resistance d

82 ovide inotropic support through reverse-mode Ca2+ entry, and/or deplete intracellular Ca2+ stores.

83 cell size and limited to cells with similar Ca2+ entry (approximately 150 x 10(6) Ca2+ ions/pF cell

84 ellular stores, but their roles in mediating Ca2+ entry are unclear.

85 release from internal stores and persistent Ca2+ entry at the plasma membrane.

86 ns if they were briefly depolarized to allow Ca2+ entry before stimulation.

87 in NHK and M-1 cells that were treated with Ca2+ entry blockers allowed cAMP activation of the B-Raf

88 Nevertheless, OAG-induced Ca2+ entry bore the hallmarks of TRPC6 function; it was

89 PM2 short variant (TRPM2-S) in mediating the Ca2+ entry burst required for induction of endothelial c

90 Inactivation of Ca-channels will also limit Ca2+ entry, but it remains unclear whether G-proteins ca

91 Neither phase of HPV requires voltage-gated Ca2+ entry, but SOCE contributes to phase 2.

92 However, activation of receptor-operated Ca2+ entry by oleoyl-2-acetyl-sn-glycerol, the membrane

93 membrane of stomatal guard cells, promoting Ca2+ entry by shifting the voltage-sensitivity of the ch

94 the full-length TRPM2 enhanced H2O2-mediated Ca2+ entry, cationic current, and the transendothelial e

95 , which contribute to increased capacitative Ca2+ entry (CCE) and DNA synthesis.

96 Capacitative Ca2+ entry (CCE) has been speculated to contribute to Ca

97 acellular Ca2+ store depletion (capacitative Ca2+ entry, CCE) represents the preferential Ca2+ source

98 TRPC gene family of putative store-operated Ca2+ entry channels contributes to the increase in micro

99 lease and the activation of "store-operated" Ca2+ entry channels is an important but so far poorly un

100 elective (ARC) channels - receptor-activated Ca2+ entry channels whose activation is entirely indepen

101 The absence of voltage-dependent Ca2+ entry channels, which emerge later, indicates that

102 idates for capacitative and non-capacitative Ca2+ entry channels.

103 g hTRPC3 in stable form, TRPC3a gave rise to Ca2+-entry channels that are not only activated by the G

104 ed proliferation of NSC progeny, reduces the Ca2+ entry component of the Cai2+ response to bFGF witho

105 + entry (deltaF(Tot)) was separated into two Ca2+ entry components, LCC-mediated (deltaF(LCC)) and NC

106 ossess the calcium-selective, store-operated Ca2+ entry current, I(SOC).

107 The total Ca2+ entry (deltaF(Tot)) was separated into two Ca2+ ent

108 ation of Rho kinase was elicited due to both Ca2+ entry-dependent involvement of Ca2+/calmodulin-depe

109 urrent measured by patch-clamp recording and Ca2+ entry detected by intracellular fura-2 fluorescence

110 TRPM2-dependent Ca2+ entry did not influence the extent or time course o

111 2A) as critical components of store-operated Ca2+ entry downstream of STIM.

112 (TRPC) channels are an important pathway for Ca2+ entry during PASMC proliferation.

113 produce CDF, and such facilitation augments Ca2+ entry during stimulation by repetitive action-poten

114 ry few IP3Rs contribute substantially to the Ca2+ entry evoked by the BCR.

115 m [Ca2+] ([Ca2+]t-sys) allowed estimation of Ca2+ entry flux from the rate of decay of [Ca2+]t-sys.

116 dothelial cells, which can trigger augmented Ca2+ entry following Ca2+ store depletion.

117 membrane of endothelial cells, and triggers Ca2+ entry following store depletion and the resultant i

118 -type Ca2+ channels, conduits of presynaptic Ca2+ entry for evoked neurotransmission.

119 nsient Ca2+ release from internal stores and Ca2+ entry from extracellular compartment.

120 of STIM on other modes of receptor-activated Ca2+ entry have not been examined.

121 r thapsigargin also activated La3+-sensitive Ca2+ entry in a PKCalpha-dependent manner.

122 as bursting electrical activity and periodic Ca2+ entry in beta-cells.

123 ay be an important contributor to pathogenic Ca2+ entry in dystrophic mouse muscle and may have impli

124 nd thereby activates store depletion-induced Ca2+ entry in endothelial cells.

125 proposed to be essential for store-operated Ca2+ entry in endothelial cells.

126 Isotretinoin reduced Ca2+ entry in HaCaT cells and decreased survival of HaCa

127 of these channel proteins in store-operated Ca2+ entry in HEK293 cells.

128 of STIM1 inhibited TG- or agonist-dependent Ca2+ entry in HEK293 or SH-SY5Y cells.

129 ed similar non-selective cation currents and Ca2+ entry in HSY cells.

130 tion of TRPC1 is an important determinant of Ca2+ entry in human endothelial cells.

131 ired for the epidermal growth factor-induced Ca2+ entry in human glomerular mesangial cells.

132 A chief mechanism of Ca2+ entry in lymphocytes is through store-operated calc

133 , can each mediate store-depletion-activated Ca2+ entry in mammalian cells, our findings with hTRC3a

134 These results show that TRPC4-dependent Ca2+ entry in mouse LECs is a key determinant of increas

135 de novel evidence that SAH leads to enhanced Ca2+ entry in myocytes of small diameter cerebral arteri

136 ns is a potentially important determinant of Ca2+ entry in neurotransmission.

137 re-operated Ca2+ entry, a common pathway for Ca2+ entry in non-excitable tissue, is apparent in the s

138 itative and capacitative (or store-operated) Ca2+ entry in nonexcitable cells represents a switching

139 particularly with respect to store-operated Ca2+ entry in nonexcitable cells.

140 ated Ca2+ (CRAC) channels and store-operated Ca2+ entry in rat basophilic leukemia (RBL-2H3) cells.

141 examine the potential role of store-operated Ca2+ entry in regulating cardiac calcineurin activation

142 (TRPC3)-expressing cells and did not affect Ca2+ entry in response to arachidonic acid.

143 Store-operated Ca2+ entry in response to PLC-coupled receptor activatio

144 -trisphosphate receptors (IP3R), the lack of Ca2+ entry in response to receptor activation is attribu

145 c kidney (HEK) cells showed that it mediates Ca2+ entry in response to stimulation of the Gq-phosphol

146 However, store-operated Ca2+ entry in response to the pump blocker, thapsigargin

147 Such rhythmic dendritic Ca2+ entry in TC neurons during sleep-related firing pat

148 Thus, enhanced store-operated Ca2+ entry in the heart can regulate calcineurin-NFAT si

149 pathway in the activation of store-operated Ca2+ entry in the RBL-1 rat basophilic leukaemia cell-li

150 oA activation, indicating the requirement of Ca2+ entry in the response.

151 s work indicated that the non-store-operated Ca2+ entry in this cell type depends upon inositol trisp

152 Store-operated Ca2+ entry induced by Ca2+ pump blockade or in response

153 ination was observed in nonneuronal cells on Ca2+ entry induced by ionomycin.

154 e taste bud and evoke depolarization-induced Ca2+ entry into a select subset of taste cells.

155 receptor- or phospholipase C (PLC)-mediated Ca2+ entry into animal cells.

156 ur previous work suggested that steady-state Ca2+ entry into arterial myocytes, and thus global [Ca2+

157 RPC3 channels, components of agonist-induced Ca2+ entry into cells.

158 poised to enhance the transduction of local Ca2+ entry into diverse signaling pathways.

159 the rapid release of neurotransmitters after Ca2+ entry into presynaptic terminals and also appears t

160 rve impulses or chemical stimulation promote Ca2+ entry into PSNTs, including nociceptors.

161 both STIM1 and STIM2 promote store-operated Ca2+ entry into T cells and fibroblasts and that STIM pr

162 versible cell depolarization and unregulated Ca2+ entry into the cell.

163 Moreover, extracellular Ca2+ entry into the ER was evident even when intracellul

164 tube germination and elongation and blocked Ca2+ entry into the growing tip, suggesting that channel

165 Our results indicate that Ca2+ entry into the presynaptic terminals during the act

166 otion of hyperactivated spermatozoa requires Ca2+ entry into the sperm tail by an alkalinization-acti

167 ted Ca2+ entry may be an important route for Ca2+ entry into the syncytiotrophoblast of term, but not

168 ulation of T-type Ca2+ currents and enhanced Ca2+ entry into these cells could contribute to the deve

169 One important mechanism that inhibits Ca2+ entry involves binding of G-protein betagamma subun

170 To maintain Ca2+ homeostasis, Ca2+ entry is balanced by efflux mediated by the sarcole

171 In many cell types, store-operated Ca2+ entry is manifest as a non-voltage-gated Ca2+ curre

172 Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (C

173 tion potentials, suggesting that presynaptic Ca2+ entry is not primarily impaired.

174 to store-operated Ca2+ entry mechanism, the Ca2+ entry is preceded by activation of phospholipase C-

175 B activation, but the role of store-operated Ca2+ entry is unclear.

176 We propose that store-operated Ca2+ entry may be an important route for Ca2+ entry into

177 Oscillating plasma membrane Ca2+ entry may play a role in generating intracellular C

178 As the sole Ca2+ entry mechanism in a variety of non-excitable cells

179 ossibility that Ang1 acts by inhibiting this Ca2+ entry mechanism in endothelial cells.

180 According to store-operated Ca2+ entry mechanism, the Ca2+ entry is preceded by acti

181 2+ channels and by unknown receptor-operated Ca2+ entry mechanisms.

182 hippocampal neurons the relationship between Ca2+ entry, O2- production, and kinase activity.

183 ever, our results indicate that the elevated Ca2+ entry occurs through the reverse mode operation of

184 Store-operated Ca2+ entry, partially attributed to transient receptor p

185 calcium (SOC) entry represents the principal Ca2+ entry pathway into nonexcitable cells.

186 In non-excitable cells, the major Ca2+ entry pathway is the store-operated pathway in whic

187 t with the hypothesis that hTRPM3 mediates a Ca2+ entry pathway that apparently is distinct from the

188 Multiple Ca2+ entry pathways may contribute to CREB activation in

189 t apparently is distinct from the endogenous Ca2+ entry pathways present in HEK 293 cells.

190 ays and molecular identity of the associated Ca2+ entry pathways remain unclear.

191 that STIM1 is a more universal regulator of Ca2+ entry pathways than previously thought, and appears

192 We conclude that the LCC and NCX Ca2+-entry pathways interact synergistically to trigger

193 Agonist-activated Ca2+ entry plays a critical role in Ca2+ signalling in n

194 Initiation of this response required Ca2+ entry, primarily via TRPV1.

195 ctivation of local AMPA receptors suppresses Ca2+ entry (probably by silencing 20-40 P/Q-type channel

196 2+ signaling and reveal that LFA-1-dependent Ca2+ entry proceeds via a mechanism separate from store-

197 e roles of recently described store-operated Ca2+ entry proteins, Stim1 and Orai1.

198 h an HCV core (100 ng/mg) in vitro increased Ca2+ entry rate by approximately 2-fold.

199 that its principal antagonistic effect is on Ca2+ entry rather than Ca2+ release, this compound may n

200 Store-operated Ca2+ entry reflects therefore a dynamic interplay betwee

201 Rho dominant-negative mutant or C3 dampened Ca2+ entry regardless of whether Ca2+ stores were emptie

202 important physiological targets to increase Ca2+ entry remain unresolved.

203 Sustained Ca2+ entry requires endoplasmic reticulum (ER) Ca2+ depl

204 Receptor-operated Ca2+ entry (ROCE) and store-operated Ca2+ entry (SOCE) a

205 The augmented Ca2+ entry secondary to TRPC1 expression may be an impor

206 + channels are a central conduit of neuronal Ca2+ entry, so their Ca2+ feedback regulation promises w

207 been referred to variously as store-operated Ca2+ entry (SOC), capacitative Ca2+ entry, and Ca2+ rele

208 olecular components mediating store-operated Ca2+ entry (SOCE) and Ca2+ release-activated Ca2+ (CRAC)

209 x2 or Stim1 failed to trigger store-operated Ca2+ entry (SOCe) and NFAT nuclear accumulation.

210 perated Ca2+ entry (ROCE) and store-operated Ca2+ entry (SOCE) are known to be inhibited by tyrosine

211 Application of the store-operated Ca2+ entry (SOCE) blockers BTP2 (10 mum) or SKF96365 (50

212 TRPC1, a component of store-operated Ca2+ entry (SOCE) channels, is assembled in a complex wi

213 inhibitory activities toward store-operated Ca2+ entry (SOCE) in human embryonic kidney-293 cells.

214 ([Ca2+](i)), accomplished by store-operated Ca2+ entry (SOCE) involving the pore-forming ion channel

215 Store-operated Ca2+ entry (SOCE) is activated following the depletion o

216 Store-operated Ca2+ entry (SOCE) is likely the most common mode of regu

217 ncentrations are regulated by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (C

218 genes ORAI1 and STIM1 abolish store-operated Ca2+ entry (SOCE), and patients with these CRAC channel

219 d triad junctions and reduced store-operated Ca2+ entry (SOCE), which is likely due to uncoupled retr

220 P3-dependent Ca2+ release and store operated Ca2+ entry (SOCE).

221 ial role in the activation of store-operated Ca2+ entry (SOCE).

222 e-dependent Ca2+ channels and store-operated Ca2+ entry (SOCE).

223 ly in non-excitable cells, is store-operated Ca2+ entry (SOCE).

224 mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).

225 Furthermore, the increased Ca2+ entry stimulates vigorous recruitment of convention

226 These findings indicate that the Ca2+ entry supporting [Ca2+]i oscillations in HEK293 cel

227 We have investigated the nature of the Ca2+ entry supporting [Ca2+]i oscillations in human embr

228 ansgenic mice showed abundant store-operated Ca2+ entry that was inhibited with SKF96365 but not vera

229 trical activity and depolarization-dependent Ca2+ entry, these compounds may have therapeutic potenti

230 chnique to investigate the interplay between Ca2+ entries through L-type Ca2+ channels (LCCs) and rev

231 in antagonist calmidazolium, suggesting that Ca2+ entry through alpha7 nAChRs specifically enhances s

232 re-mRNA editing at Q/R site-607, which gates Ca2+ entry through AMPA receptor channels.

233 Supralinear Ca2+ events required Ca2+ entry through AMPA receptors with a subsequent Ca2+

234 hat the transient BK current is activated by Ca2+ entry through both N- and L-type Ca2+ channels.

235 Antigen stimulation of immune cells triggers Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) ch

236 Store-operated Ca2+ entry through calcium release-activated calcium cha

237 A fast transient BK current is activated by Ca2+ entry through high-threshold voltage-activated Ca2+

238 Mitochondrial trafficking is regulated by Ca2+ entry through ionotropic glutamate receptors, but t

239 rolonged AMPAR blockade acts through loss of Ca2+ entry through L-type Ca2+ channels to bring about a

240 ere dependent upon neural activity, external Ca2+ entry through L-type Ca2+ channels, and amplificati

241 als but requires membrane depolarization and Ca2+ entry through L-type Ca2+ channels.

242 Postsynaptic [Ca2+]i increases result from Ca2+ entry through ligand-gated channels, entry through

243 e, which permits some degree of reverse-mode Ca2+ entry through NCX1, as well as less efficient Ca2+

244 Ca2+ entry through NMDA receptor channels or voltage-gat

245 lso show that Reelin-induced augmentation of Ca2+ entry through NMDA receptors increases phosphorylat

246 otein kinase A (PKA)-dependent regulation of Ca2+ entry through NMDA-type glutamate receptors that wa

247 aptic plasticity--triggered, for example, by Ca2+ entry through NMDA-type glutamate receptors--only r

248 otential and, with it, the driving force for Ca2+ entry through other Ca2+-permeable pathways.

249 l, purinergic Ca2+ transients that represent Ca2+ entry through P2X receptors.

250 rom the endoplasmic reticulum (ER) activates Ca2+ entry through SOCs in the plasma membrane.

251 Our findings indicate that Ca2+ entry through store-operated Ca2+ channels leads to

252 um (ER) stores, thereby triggering sustained Ca2+ entry through store-operated Ca2+ release-activated

253 Stimulation of immune cells triggers Ca2+ entry through store-operated Ca2+ release-activated

254 he nonselective cation channel that mediates Ca2+ entry through store-operated channels (SOCs) in hum

255 Here we report that Ca2+ entry through store-operated CRAC (Ca2+ release-act

256 atory Ca2+ signals and specifically activate Ca2+ entry through the ARC channels fail to increase cal

257 ty, which would otherwise be overshadowed by Ca2+ entry through the host channel.

258 rthermore, we show that muscle APs depend on Ca2+ entry through the L-type Ca2+ channel EGL-19 with a

259 ardiac myocyte contractility is initiated by Ca2+ entry through the voltage-dependent L-type Ca2+ cha

260 ms controlling channel activity and coupling Ca2+ entry through these channels to cellular responses

261 Priming the stores with Ca2+ entry through voltage dependent channels modulated

262 This causes Ca2+ entry through voltage-gated Ca2+ channels.

263 tracellular Ca2+ sensor to feedback-regulate Ca2+ entry through voltage-gated Ca2+ channels.

264 s downstream of the well known inhibition of Ca2+ entry through voltage-gated calcium channels.

265 Ca2+ entry through voltage-gated channels, activated by

266 Ca2+ entry through voltage-gated L-type Ca2+ channels tr

267 We also show that Ca2+ entry through xCNGCs is required to mediate the rep

268 ction may be a general mechanism for linking Ca2+ entry to enhanced kinase activity and therefore to

269 s a voltage-gated Ca2+ channel that controls Ca2+ entry to mediate the hyperactivated motility needed

270 ciated with this induction in store-operated Ca2+ entry, TRPC3 transgenic mice showed increased calci

271 brane potential to negative potentials where Ca2+ entry via I(CatSper) is maximized.

272 endoplasmic reticulum stores, and subsequent Ca2+ entry via lanthanum-sensitive store-operated Ca2+ c

273 To test the role of Ca2+ entry via NCX during ischemia and reperfusion, we s

274 Consistent with Ca2+ entry via NCX during ischemia, we found that hearts

275 ischemia-reperfusion injury, suggesting that Ca2+ entry via reverse-mode NCX is a major cause of isch

276 borate, which suggests that they are due to Ca2+ entry via store-operated channels.

277 nel blockade and is essential for subsequent Ca2+ entry via the L-type Ca2+ channel.

278 LC)-IP3 pathway that activates extracellular Ca2+ entry via the plasmalemmal store-operated channel t

279 We further showed that Rho-activated Ca2+ entry via TRPC1 is important in the mechanism of th

280 elial permeability through the activation of Ca2+ entry via TRPM2.

281 len, as well as the absence of swelling when Ca2+ entry was abolished, indicate an essential role for

282 Ca2+ entry was associated with a distinct nonselective c

283 Importantly, OAG-induced Ca2+ entry was blocked by the potent L-type Ca2+ channel

284 l, compared with the wild-type channel, when Ca2+ entry was normalized to cell size and limited to ce

285 ated in PE cells, whereas agonist-stimulated Ca2+ entry was reduced in cells from PE compared with no

286 Although total Ca2+ entry was slightly larger for the synprint deletion

287 Store-operated Ca2+ entry was stimulated using 1 microM thapsigargin in

288 TRPC6 knockdown, whereas vasopressin-induced Ca2+ entry was suppressed by more than 50%.

289 led that thapsigargin-induced store-operated Ca2+ entry was unaffected by TRPC6 knockdown, whereas va

290 els thought to be involved in store-operated Ca2+ entry, was also studied at the mRNA and protein lev

291 genes that alter thapsigargin (TG)-dependent Ca2+ entry, we discovered a required and conserved role

292 Although the total and NCX-mediated Ca2+ entries were increased again, deltaF(Tot) did not s

293 Trans-sarcolemmal Ca2+ entries were measured fluorometrically in myocytes

294 Phosphorylation of TRPC1 and the resulting Ca2+ entry were essential for the increase in permeabili

295 Cell volume, pHi, ATP levels and passive Ca2+ entry were not affected by CDNB.

296 ndicate that caveolae are preferred sites of Ca2+ entry when Ca2+ stores in the endoplasmic reticulum

297 ectively blocked hormone secretion distal to Ca2+ entry, whereas the cross-coupling to G i/o proteins

298 Hypotonicity also activated Ca2+ entry, which was required for subsequent RVD.

299 th muscle cells, BTP2 blocked store-operated Ca2+ entry within 10 min with an IC50 of 0.1-0.3 microM.

300 d with downstream IP3-dependent plasmalemmal Ca2+ entry without affecting the release of intracellula