ライフサイエンスコーパス: Ca2 influx

1 to increased background cation currents and Ca2+ influx.

2 dependent [Ca2+]i increase and extracellular Ca2+ influx.

3 V), a stage corresponding to CtxB-stimulated Ca2+ influx.

4 bAP amplitude and an increase of concurrent Ca2+ influx.

5 AP-CSD also suppressed thapsigargin-induced Ca2+ influx.

6 PC1 and its consequences on thrombin-induced Ca2+ influx.

7 rovides an electrochemical gradient to drive Ca2+ influx.

8 dentify proteins that inhibit store-operated Ca2+ influx.

9 quence markedly reduced the thrombin-induced Ca2+ influx.

10 in dose-dependent transient increases in net Ca2+ influx.

11 d voltage-activated Ca2+ current and lowered Ca2+ influx.

12 ble to sweet or bitter stimulation, required Ca2+ influx.

13 maller ICa density, which should both reduce Ca2+ influx.

14 iption but is not dependent on voltage-gated Ca2+ influx.

15 of NMDA receptors, resulting in excitotoxic Ca2+ influx.

16 a plays a role in PMA-mediated inhibition of Ca2+ influx.

17 context for cADPR as a second messenger for Ca2+ influx.

18 ggered secretion by modulating voltage-gated Ca2+ influx.

19 taneous and high K+-stimulated voltage-gated Ca2+ influx.

20 spikes (LTS) accompanied by global dendritic Ca2+ influx.

21 more, these channels are responsible for the Ca2+ influx.

22 and contributes to carbachol-stimulation of Ca2+ influx.

23 (v)beta(3) receptors by vitronectin triggers Ca2+ influx.

24 stores in neurons by depolarization without Ca2+ influx.

25 FKBP12 occurs, possibly due to the increased Ca2+ influx.

26 ol and OAG, but not thapsigargin, stimulated Ca2+ influx.

27 rtially OFF but inducible by elevated global Ca2+ influx.

28 bsence of the Na+-Ca2+ exchanger by limiting Ca2+ influx.

29 y inhibiting the Trpc3-mediated component of Ca2+ influx.

30 vation, and limiting increased intracellular Ca2+ influx.

31 on-CF and CF airway epithelia by attenuating Ca2+ influx.

32 is subsequently induced by voltage-dependent Ca2+ influx.

33 when cells were stimulated in the absence of Ca2+ influx.

34 ed and required NMDA receptor activation and Ca2+ influx.

35 by displacing alpha-actinin from NR1 C0 upon Ca2+ influx.

36 synaptic depolarization induces calcium ion (Ca2+) influx.

37 +) T cells had reduced cAMP accumulation and Ca2(+) influx.

38 ough the ATP-gated P2x7 receptor controlling Ca2(+) influx.

39 cytic AMPARs and mGluRs caused extracellular Ca2+ influx, a Ca2+/protein kinase C-dependent increase

40 sence of NSAIDs is due to the stimulation of Ca2+ influx across the cytoplasmic membrane, which resul

41 from the endoplasmic reticulum, followed by Ca2+ influx across the plasma membrane.

42 er) rely on membrane depolarization to drive Ca2+ influx across the plasma membrane.

43 This suggests a mechanism whereby Ca2+ influx acting via CaM and NINAC accelerates the bin

44 t an adaptation model whereby TRPM8-mediated Ca2+ influx activates PLC, thereby decreasing PIP2 level

45 20/Claudin proteins, but did not require its Ca2+ influx activity.

46 tion of the NMDA glutamate receptor subtype, Ca2+ influx, activity of CaM kinase II, and function of

47 Ca2+ influx also promotes translocation of cytosolic 5-l

48 Postsynaptic Ca2+ influx also stimulates local synaptic differentiati

49 -methyl-D-aspartate (NMDA) receptor-mediated Ca2+ influx and actin polymerization.

50 art failure and death associated with excess Ca2+ influx and acute beta-adrenergic receptor stimulati

51 rect mechanistic link between NMDAR-mediated Ca2+ influx and AMPAR endocytosis.

52 oteins that are essential for store-operated Ca2+ influx and Ca2+ release-activated Ca2+ (CRAC) chann

53 , and expression of wild-type Orai1 restored Ca2+ influx and CRAC channel activity in patient T cells

54 e hyperpolarization and potentiation of both Ca2+ influx and degranulation.

55 owed a matching axonal gradient, with higher Ca2+ influx and exocytosis at distal boutons.

56 annel inhibitors block growth factor-induced Ca2+ influx and fibroblast cell migration.

57 alized Kv3 channels keep APs brief, limiting Ca2+ influx and hence release probability, thereby influ

58 signaling pathway prevented the VEGF-induced Ca2+ influx and hyperpermeability similar to the inhibit

59 vation events are intact in these cells, but Ca2+ influx and IL-2 gene transcription are defective.

60 strated that Ang1 inhibited the VEGF-induced Ca2+ influx and increase in endothelial permeability in

61 about effects of FHM1 mutations on neuronal Ca2+ influx and inhibitory and excitatory neurotransmiss

62 ing agents promote beta-cell depolarization, Ca2+ influx and insulin secretion.

63 ressive compound that potently inhibits both Ca2+ influx and interleukin-2 (IL-2) production in lymph

64 the command signal, demonstrated that total Ca2+ influx and myocyte shortening were larger in respon

65 Both Ca2+ influx and neurite induction were blocked by TRPC5

66 PLC, and PI(3)K suppressed both CtxB-induced Ca2+ influx and neurite outgrowth.

67 isplayed significantly decreased TCR-induced Ca2+ influx and nuclear factor of activated T cells (NFA

68 However, these differences in Ca2+ influx and nuclear factor of activated T cells (NFA

69 , MTMR6 functions as a negative regulator of Ca2+ influx and proliferation of reactivated human CD4 T

70 ade of depression is mediated by presynaptic Ca2+ influx and protein kinase C (PKC) and requires loca

71 etory defect was distal to glucose-dependent Ca2+ influx and resulted from reduced proinsulin biosynt

72 e the consequence of mechanisms that involve Ca2+ influx and signalling rather than gross changes in

73 rai1 in SCID T cells restores store-operated Ca2+ influx and the CRAC current (I(CRAC)).

74 RGDSP-induced Ca2+ response was unrelated to Ca2+ influx and the inositol triphosphate receptor-gated

75 -activated K+ channel KCa3.1 is required for Ca2+ influx and the subsequent activation of B and T cel

76 inotropic effect via inhibiting sarcolemmal Ca2+ influx and the subsequent increase in intracellular

77 ecause of the nonlinear relationship between Ca2+ influx and transmitter release, CDI and CDF are pow

78 ring persistent Ca2+ sparklets that increase Ca2+ influx and vascular tone.

79 companied by inhibition of voltage-dependent Ca2+ influx and was recapitulated by incubation of neuro

80 a voltage jump protocol to rapidly increase Ca2+ influx, and could be fitted with a single time cons

81 acts with L-type calcium channels, regulates Ca2+ influx, and defends against Leishmania major infect

82 ne potential depolarization, increased islet Ca2+ influx, and enhanced second-phase GSIS.

83 e (NMDA)-type glutamate receptors, excessive Ca2+ influx, and formation of nitric oxide (NO) via neur

84 , leading to plasma membrane depolarization, Ca2+ influx, and increased chemosensory fiber discharge.

85 (GLP-1) stimulates cAMP production, promotes Ca2+ influx, and mobilizes an intracellular source of Ca

86 human Orai1, greatly diminish store-operated Ca2+ influx, and primary T cells ectopically expressing

87 cardiac pathology despite large increases in Ca2+ influx, and they were even partially resistant to p

88 ially as the magnitudes of LTF and increased Ca2+ influx are positively correlated.

89 is accompanied by reduced NMDAR current and Ca2+ influx, as well as reduced voltage-gated sodium cur

90 nce supporting this 'Ca2+ sparklet' model of Ca2+ influx at a physiological membrane potential and ex

91 yridine-sensitive (i.e. L-type Ca2+ channel) Ca2+ influx at a physiologically relevant membrane poten

92 r guidance cues on axon pathfinding requires Ca2+ influx at the growth cone, but how activation of gu

93 ular guidance factors, many of which trigger Ca2+ influx at the growth cone; however, the identity of

94 ns, as a part of a protein complex, modulate Ca2+ influx at the plasma membrane and along OL processe

95 ntracellular free Ca2+ was due to changes in Ca2+ influx but not efflux, as observed in extracellular

96 ming required for coupling vesicle fusion to Ca2+ influx, but Ca2+ binding by both C2 domains is requ

97 elective (CAN) cation channel that decreases Ca2+ influx by depolarizing lymphocytes.

98 itch opened the TRPM2 channel to allow large Ca2+ influx by releasing TRPM2-S inhibition of TRPM2, wh

99 In support of this idea, limiting Ca2+ influx by using weaker depolarizing stimuli promote

100 + : H+ ratio is 1 : 2, ensuring that after a Ca2+ influx [Ca2+]i recovery is not influenced by the me

101 ys regulating NFAT subcellular localization (Ca2+ influx, Ca2+-calmodulin-calcineurin signalling and

102 g in subcellular domains of nearly continual Ca2+ influx called 'persistent Ca2+ sparklets'.

103 it functions to regulate membrane potential, Ca2+ influx, cell volume, and chloride secretion.

104 tial (canonical) channel (TRPC) 3 is a major Ca2+ influx channel in pancreatic and salivary gland cel

105 How STIM1 activates the Ca2+ influx channels and whether STIM1 contributes to th

106 a2+ from intracellular stores and opening of Ca2+ influx channels on the plasma membrane.

107 distance between G2AeNOS and plasma membrane Ca2+ influx channels.

108 nnel blocker Gd3+ prevented H2O2-induced net Ca2+ influx, consistent with application of exogenous H2

109 e ability to release [3H]norepinephrine in a Ca2+ influx-dependent manner in response to PACAP.

110 lted in outgrowth of axon-like neurites in a Ca2+ influx-dependent manner.

111 PAR endocytosis, indicating a requirement of Ca2+ influx directly through the NMDAR channels.

112 It is natural to assume that the increased Ca2+ influx during action potentials is directly respons

113 fedipine, indicating that they resulted from Ca2+ influx during electrical activity, and occurred at

114 Further Ca2+ influx during paired-pulse stimuli then leads to de

115 is a powerful mechanism for up-regulation of Ca2+ influx during repeated membrane depolarization.

116 This increase in Ca2+ influx enhanced interleukin-2 production.

117 NMDA receptor-mediated postsynaptic Ca2+ influx enhances AMPAR internalisation, but the mole

118 Both Ca2+ influx evoked by bFGF and NSC proliferation are att

119 ined three-dimensional diffusion modeling of Ca2+ influx-exocytosis coupling was consistent with clus

120 ximal ones, probably attributable to greater Ca2+ influx for distal boutons.

121 rough PIP(2) to enhance both plasma membrane Ca2+ influx from the extracellular space, as well as ino

122 that SS Ca2+ sparks are under the control of Ca2+ influx from the extracellular space.

123 ivated outward current that was dependent on Ca2+ influx I(K(Ca).

124 ntial cation channels to attenuate cytosolic Ca2+ influx, implicating a mechanism by which overexpres

125 ing of the firing patterns and regulation of Ca2+ influx in a variety of neurons.

126 I(3)P phosphatase MTMR6 in the regulation of Ca2+ influx in activated CD4 T cells and suggest that MT

127 ype Ca2+ channels to action potential-evoked Ca2+ influx in dendritic spines of CA1 pyramidal neurons

128 We evaluated the possibility that Ca2+ influx in enamel cells might be mediated by SOCE an

129 predominantly responsible for store-operated Ca2+ influx in human embryonic kidney 293 cells and huma

130 These data indicate that Ca2+ influx in LS8 cells and enamel organ cells is media

131 tems, which permeabilize membranes and cause Ca2+ influx in mammalian cells, promote lysosomal exocyt

132 ROS are involved in the effects of AngII on Ca2+ influx in NTS neurons receiving vagal afferents and

133 dent, the molecular basis for AMPAR-mediated Ca2+ influx in OLs remains largely unclear.

134 The priming by prior Ca2+ influx in P/Q-type Ca2+ channels may determine the

135 6 expression and decreased agonist-activated Ca2+ influx in PASMCs of IPAH patients harboring the -25

136 ed K+ channel, KCa3.1, which is critical for Ca2+ influx in reactivated naive T cells and central mem

137 19 processes revealed higher-amplitude local Ca2+ influx in regions with elevated levels of golli.

138 y discovered signal transducer that triggers Ca2+ influx in response to receptor-mediated depletion o

139 lular concentration of potassium or blocking Ca2+ influx in SCN cultures by lowering [Ca2+], reversib

140 al co-activators of TRPM2 that contribute to Ca2+ influx in T lymphocytes and presumably other cell t

141 isely reproducible timing and second, slower Ca2+ influx in the cation-permeable sEPSC channel.

142 role of NMDAR subtypes and of NMDAR-mediated Ca2+ influx in the NMDAR-induced endocytosis of GluR2-co

143 channels are the major source of bAP-evoked Ca2+ influx in these structures.

144 cycle machinery, the processes that regulate Ca2+ influx in this context have not been fully elucidat

145 te to resting membrane conductance and basal Ca2+ influx in vascular myocytes.

146 rbol 12 myristate 13-acetate (PMA) inhibited Ca2+ influx in wild-type but not PKC-theta-/- T cells, s

147 the role of membrane potential and calcium (Ca2+) influx in the expression of the circadian rhythm o

148 rane helices 1 and 3, respectively, diminish Ca2+ influx, increase current carried by monovalent cati

149 It is likely that mitochondrial Ca2+ influx increases the dynamic response range of the

150 mbrane and reversed its inhibitory action on Ca2+ influx, indicating that membrane association of gol

151 nstrate that Ang1 blocks the TRPC1-dependent Ca2+ influx induced by VEGF by interfering with the inte

152 entricular myocytes because of reductions in Ca2+ influx induced in part by alterations in early repo

153 Enhanced Ca2+ influx-induced cellular necrosis and cardiomyopathy

154 sition pore that underpins necrosis, blocked Ca2+ influx-induced necrosis of myocytes, heart failure,

155 Ca2+ influx induces a release of Ca2+ from the sarcoplas

156 ulmonary arterial myocytes and transmembrane Ca2+ influx into carotid body glomus cells.

157 s both synaptic- and action potential-evoked Ca2+ influx into dendritic spines by approximately 50%.

158 of ducts and acini; and (ii) OAG stimulated Ca2+ influx into dispersed ductal cells.

159 Since excessive Ca2+ influx into neurons is a crucial step for excitotox

160 d that K+ channels play an important role in Ca2+ influx into T lymphocytes by helping to maintain a

161 ed reactive oxygen species (ROS) stimulate a Ca2+ influx into the cytoplasm that is required for root

162 ne potential and maximizes the conversion of Ca2+ influxes into possible pH signals.

163 roM PGF(2alpha) cause a TP receptor-mediated Ca2+ influx involving both L-type Ca2+ channels and a re

164 set the cell membrane potential and regulate Ca2+ influx, ion channels play a critical role in mast c

165 (NCX-KO) and demonstrated that reverse-mode Ca2+ influx is absent in the NCX-KO myocytes.

166 While Ca2+ influx is essential for activation of the cell cycl

167 Ca2+ influx is essential for many cellular functions, fr

168 this study, we demonstrate that CtxB-induced Ca2+ influx is mediated by TRPC5 channels, naturally exp

169 Ca2+ influx is negatively regulated by Ca2+ -activated K

170 partmentalize signaling events downstream of Ca2+ influx is not known.

171 The enhancing effect of PKC-theta on Ca2+ influx is not only dependent on the strength of TCR

172 A common mechanism for Ca2+ influx is store-operated Ca2+ entry (SOCE).

173 itary lactotrophs, spontaneous voltage-gated Ca2+ influx is sufficient to maintain prolactin release

174 of stretch-activated channels, we show that Ca2+ influx is triggered by hypotonic solutions, which c

175 dritic plateau potentials produce widespread Ca2+ influx, large after-depolarizations, burst firing o

176 concentration near the interface, indicating Ca2+ influx localized at the T cell/dendritic cell conta

177 Mitochondrial Ca2+ influx may be fast enough for this role.

178 by a combination of electrical recording and Ca2+ influx measurements in rat hippocampal neurons in c

179 current, to investigate whether this type of Ca2+ influx mechanism regulates the cardiac hypertrophic

180 age but greatly sensitizes the force-sensing Ca2+-influx mechanism.

181 TRPC3-mediated Ca2+ influx mediates damage to pancreas and salivary gla

182 Excessive Ca2+ influx mediates many cytotoxic processes, including

183 Ca2+ influx mediates T cell function and immunity to inf

184 inhibitor of K(ATP) channels that stimulates Ca2+ influx, modulates [3H]thymidine incorporation.

185 tivation of NMDA receptors and corresponding Ca2+ influx, MyoVb associates with recycling endosomes (

186 2+](i) suggested that most CICR triggered by Ca2+ influx occurred away from the plasma membrane.

187 , but not 4alpha-PMA, mimicked the effect of Ca2+ influx on F-actin.

188 protein kinase kinase beta downstream of the Ca2+ influx or knockdown of the downstream Ca2+/calmodul

189 ein (GFP) fusion gene (Adbeta2a) to increase Ca2+ influx or with AdGFP as a control.

190 re not significantly affected, and the major Ca2+ influx pathway in lymphocytes, ICRAC, is blocked on

191 le of store-, receptor- and voltage-operated Ca2+ influx pathways in rat intrapulmonary arteries (IPA

192 calcium entry indicating a direct effect on Ca2+ influx pathways.

193 activation of plasma membrane Gd3+-sensitive Ca2+-influx pathways.

194 Pretreatment with CP for 1 h prevented Ca2+ influx, proteolytic activities, and apoptosis in RG

195 show that increase of cellular Ca2+ through Ca2+ influx, rather than Ca2+ release from intracellular

196 cated that golli produced its effect through Ca2+ influx, rather than Ca2+ release from intracellular

197 the mechanisms of gating of the supranormal Ca2+ influx required for initiating of apoptosis are not

198 We propose that periodic Ca2+ influx, resulting from circadian variations in memb

199 Inhibitors of Ca2+ influx, SR Ca2+ uptake and release, mitochondrial C

200 ich was essential for the action of golli on Ca2+ influx, suggesting that binding of golli to the pla

201 pholipase C, IP3 receptors, Ca2+ stores, and Ca2+ influx, suggesting the involvement of transient rec

202 ility changes in eukaryotic cells, causing a Ca2+ influx that drives cell death pathways.

203 The Ca2+ influx that follows PLC activation is likely mediat

204 both positively and negatively regulate the Ca2+ influx that is critical for NFAT activity.

205 C family may serve as a key mediator for the Ca2+ influx that regulates axon guidance during developm

206 trations of cyclopiazonic acid revealed that Ca2+ influx that regulates CICR is associated with a sel

207 In this state, upon Ca2+ influx the protein will bind the three Ca2+ ions im

208 which is not activated directly by external Ca2+ influx, then acts as a downstream effector of relea

209 ng from A2A-coupled KCa channels facilitates Ca2+ influx, thereby activating eNOS and NO release.

210 can be differentially released with varying Ca2+ influx, thereby increasing the range of potential s

211 distinct ion channels on the sensory cilia: Ca2+ influx through a cyclic nucleotide-gated (CNG) chan

212 The first phase resulted from Ca2+ influx through AMPA receptors, whereas the second p

213 s B subunit of cholera toxin (CtxB), induced Ca2+ influx through an unidentified, voltage-independent

214 release from amacrine cells is triggered by Ca2+ influx through both voltage-gated Ca2+ (Ca(v)) chan

215 eptors, which are activated independently by Ca2+ influx through Ca(v) channels and NMDARs, respectiv

216 l approaches in zebrafish, demonstrated that Ca2+ influx through CaV1.2 regulates jaw development.

217 How abnormal Ca2+ influx through CaV1.2 underlies phenotypes such as

218 his stimulatory effect was dependent on both Ca2+ influx through cGMP-gated channels and phosphorylat

219 es, and thus global [Ca2+]i, is regulated by Ca2+ influx through clusters of L-type Ca2+ channels ope

220 Ca2+ influx through CRAC channels can therefore activate

221 gulated, accompanied by a marked increase in Ca2+ influx through CRAC channels.

222 whereas global Ca2+ signals were mediated by Ca2+ influx through dendritic, voltage-dependent Ca2+ ch

223 ese receptor subunits strongly suggests that Ca2+ influx through GluR2-lacking AMPARs may play an imp

224 ctivity triggers a novel type of plasticity: Ca2+ influx through GluR2-lacking synaptic AMPARs drives

225 ostsynaptic terminal and selectively reports Ca2+ influx through glutamate receptors (GluRs) with sin

226 This facilitation occurs when local Ca2+ influx through individual channels selectively acti

227 des: (1) completely "ON" and driven by local Ca2+ influx through individual channels, (2) completely

228 edge contraction is critically regulated by Ca2+ influx through L-type Ca2+ channels in growth facto

229 oplasmic reticulum Ca2+ release, rather than Ca2+ influx through L-type Ca2+ channels, is the target

230 II was independent of pressure but required Ca2+ influx through L-type Ca2+ channels.

231 oplasmic reticular Ca2+ release triggered by Ca2+ influx through L-type Ca2+ channels.

232 al. in this issue of Neuron demonstrate that Ca2+ influx through L-type channels elevates dopamine sy

233 of the transcription factor NFATc4 via local Ca2+ influx through L-type channels requires AKAP79/150,

234 Ca2+ influx through NMDA receptors (NMDARs) leads to cha

235 l activation and the subsequent reduction in Ca2+ influx through NMDARs and L-type VGCCs results in a

236 PKA blockers reduced the relative fractional Ca2+ influx through NMDARs as determined by reversal pot

237 Blocking Ca2+ influx through other channel types has little or op

238 I(am-s)-inhibiting P2X ion channels but also Ca2+ influx through P2X4 and P2X(4/6) ion channels.

239 Ca2+ influx through plasma membrane lesions triggers a r

240 ced a PKA- and A2AR-independent reduction in Ca2+ influx through R-type voltage-gated Ca2+ channels.

241 express Ca2+ -handling molecules and mediate Ca2+ influx through SOCE.

242 Here we show that inhibiting Ca2+ influx through stretch-activated channels using var

243 Ca2+ influx through synaptic NMDA receptors (NMDA-Rs) tr

244 These data demonstrate that Ca2+ influx through T-type Ca2+ channels, followed by Ca

245 nge, endothelin also inhibited voltage-gated Ca2+ influx through the G i/o signaling pathway.

246 se results show that persistent increases in Ca2+ influx through the I(Ca-L) enhance contractility bu

247 Increases in Ca2+ influx through the L-type Ca2+ channel (LTCC, Cav1.

248 r hypothesis is that persistent increases in Ca2+ influx through the LTCC cause apoptosis if the exce

249 Ca2+ influx through the N-methyl-d-aspartate (NMDA)-type

250 mouse neurotoxin-based model of PD, reduced Ca2+ influx through transient receptor potential C1 (TRP

251 Our aim was to determine if Ca2+ influx through transient receptor potential canonic

252 Ca2+ influx through TRPC channels expressed after MI act

253 al responses of the growth cone to BMP7, and Ca2+ influx through TRPC tilts the LIMK-SSH balance towa

254 Excessive Ca2+ influx through TRPV4 predisposes RGCs to activation

255 e, rapid, global Ca2+ flashes that represent Ca2+ influx through VDCCs during action potentials, and

256 ts indicated that these events are caused by Ca2+ influx through VDCCs during action potentials.

257 We tested the hypothesis that Ca2+ influx through VGCCs regulates SMC differentiation

258 These results indicate that Ca2+ influx through VGCCs, activated after action potent

259 Inhibition of Ca2+ influx through voltage-dependent Ca2+ channels usin

260 tips of the dendritic branches and increased Ca2+ influx through voltage-gated Ca2+ channels.

261 nization in salamander retina and found that Ca2+ influx through voltage-gated L-type channels causes

262 Finally, although Ca2+ influx through voltage-operated calcium channels do

263 emonstrate that postsynaptic calcium 2+ ion (Ca2+) influx through glutamate receptors and subsequent

264 Calcium (Ca2+) influx through NMDA receptors (NMDARs) is essentia

265 olic inhibition was associated with enhanced Ca2+-influx through NMDA receptors, which when blocked r

266 findings indicate that NCX KO myocytes limit Ca2+ influx to &20% of that in WT by reducing ICa and by

267 Ca2+ influx triggered by action potential waveforms was

268 Ca2+ influx triggers distinct features of CaMKII targeti

269 l insulin 1 (INS1) cells for which localized Ca2+ influx triggers exocytosis with high probability an

270 Selective blockade of glucose-stimulated Ca2+ influx unmasked a protein kinase A (PKA)-sensitive

271 depletion of ER Ca2+ stores, STIM2 activated Ca2+ influx upon smaller decreases in ER Ca2+.

272 naling, which controls stuttering persistent Ca2+ influx, vascular tone, and blood pressure under phy

273 STIM2, like STIM1, caused Ca2+ influx via activation of the plasma membrane Ca2+ c

274 g that these responses require extracellular Ca2+ influx via channels other than voltage-dependent Ca

275 y stabilizing GluA1 phosphorylation; and (3) Ca2+ influx via CPARs restores CREB phosphorylation as a

276 otentials depolarize the membrane and induce Ca2+ influx via high-voltage-activated Ca2+ channels (I(

277 lying a KO AP waveform voltage clamp reduced Ca2+ influx via ICa by 59% compared with WT AP waveform

278 In principle, higher Ca2+ influx via ICa,L should be balanced by higher efflu

279 We first examined whether IL-6 reduced Ca2+ influx via L-type Ca2+ -channel current (ICa,L).

280 ility density approach to modeling localized Ca2+ influx via L-type Ca2+ channels and Ca2+-induced Ca

281 own-regulation of the beta1 subunit required Ca2+ influx via L-type Ca2+ channels.

282 Membrane depolarization increased Ca2+ influx via low-activity and high-activity persisten

283 SD peptide markedly reduced thrombin-induced Ca2+ influx via SOC in HPAECs in contrast to control pep

284 domain interaction with TRPC1 in regulating Ca2+ influx via SOC.

285 Our findings demonstrate that Ca2+ influx via store-operated CRAC channels is essentia

286 ttenuates thrombin- and thapsigargin-induced Ca2+ influx via store-operated TRPC1 channels.

287 ovide evidence for a novel mechanism whereby Ca2+ influx via VGCCs stimulates expression of SMC diffe

288 Second, when Ca2+ influx was enhanced during trains, train estimates

289 The Ca2+ influx was inhibited by the L-type Ca2+ channel ant

290 Plasma membrane Ca2+ influx was measured by Mn2+ quench rates of fura2-f

291 Ca2+ influx was significantly higher in keratinocytes ob

292 [Ca2+]i), which are driven by store-operated Ca2+ influx, were transformed into a sustained elevation

293 Both receptors mediate Ca2+ influx whereas muscarinic receptors may also recrui

294 r STIM1 had severely impaired store-operated Ca2+ influx, whereas deficiency in the calcium sensor ST

295 -coupled KATP-channel activation facilitates Ca2+ influx which may cause some stimulation of endothel

296 hat TRPC1 contributes to bFGF/FGFR-1-induced Ca2+ influx, which is involved in self-renewal of embryo

297 xM1 demonstrated enhanced glucose-stimulated Ca2+ influx, which resulted in improved glucose toleranc

298 sed TRPC1 levels and thapsigargin-stimulated Ca2+ influx, which was blocked by store-operated calcium

299 Blocking Ca2+ influx with nifedipine (1 muM) or levcromakalim (10

300 of Na+/Ca2+ exchange blocks this additional Ca2+ influx without affecting LTF, showing that LTF is n