ライフサイエンスコーパス: calcium influx

1 , revealing two stereotyped phases of axonal calcium influx.

2 ent thrombin permeabilization by obstructing calcium influx.

3 that it was not secondary to a reduction of calcium influx.

4 slocation and ISR, independent of effects on calcium influx.

5 disulphide bonds, which results in sustained calcium influx.

6 propagated via the innexin INX-16, likely by calcium influx.

7 dent inactivation (CDI) and allows sustained calcium influx.

8 ir direct membrane interaction and resultant calcium influx.

9 ysin deletion involves prevention of reduced calcium influx.

10 ene, which also inhibited Nod-factor-induced calcium influx.

11 pletes ER calcium, which ultimately leads to calcium influx.

12 e secretion without changes to extracellular calcium influx.

13 phosphatase SHP-1 recruitment but increased calcium influx.

14 ) 4b, a membrane glycoprotein that regulates calcium influx.

15 exchanger (NCX) as predominant mechanisms of calcium influx.

16 nhibited TRPV3-mediated membrane current and calcium influx.

17 ally mediated by TRPM4 channels activated by calcium influx.

18 in addition to the inhibition of presynaptic calcium influx.

19 bility by controlling membrane potential and calcium influx.

20 TRPC6 promoter activity and TRPC6-dependent calcium influx.

21 habditis elegans, is mediated by presynaptic calcium influx.

22 sensory neurons, which enhances sugar-evoked calcium influx.

23 and GABA) for rapid modulation of dendritic calcium influx.

24 es including the cytoskeleton remodeling and calcium influx.

25 e also as signaling molecules presumably via calcium influx.

26 the face of decreased oxygen consumption and calcium influx.

27 7 synergistically enhanced degranulation and calcium influx.

28 mpartmentalization of NMDA receptor-mediated calcium influx.

29 to action potential broadening and increased calcium influx.

30 such as neurotransmitter release by limiting calcium influx.

31 inding proteins, and was highly dependent on calcium influx.

32 T cell effector functions require sustained calcium influx.

33 istance to NMDA-induced toxicity and reduced calcium influx.

34 ired for acidosis-mediated signaling through calcium influx.

35 ering, or decreasing action potential-evoked calcium influx.

36 triggers an inward current concomitant with calcium influx.

37 subunit of PI3K and AKT as well as abrogated calcium influx.

38 esting that ASIC1 may regulate mitochondrial calcium influx.

39 elium of Young in conjunction with twice the calcium influx.

40 The calcium influx accompanying such signaling opens calcium

41 that ICWs were initiated by an extracellular calcium influx across the cell membrane nearest to the j

42 is expressed in cardiomyocytes and decreases calcium influx across the L-type Ca(2+) channel.

43 urons from young and aged rats, we show that calcium influx across the plasma membrane increases with

44 ese has been used for indirect monitoring of calcium influx across the sarcolemma and may allow detec

45 Cytosolic calcium influx activates signaling pathways known to sup

46 tance, resulting in membrane depolarization, calcium influx, aldosterone production, and cell prolife

47 ffect requires cold-induced, TRPA-1-mediated calcium influx and a calcium-sensitive PKC that signals

48 le processes, the enhancement of presynaptic calcium influx and a RIM-dependent modulation of the RRP

49 curs only in excitatory neurons and requires calcium influx and calcineurin activation.

50 her these Nod-factors differentially induced calcium influx and calcium spiking.

51 iking activity in coupled neurons depends on calcium influx and calcium-initiated signalling pathways

52 Moreover, altered calcium influx and calpain II protease activation leads

53 However, the cellular mechanisms whereby calcium influx and CaMKII control Ras activity remain el

54 els is critical for feedback control of both calcium influx and cell excitability.

55 n mediating antigen-stimulated extracellular calcium influx and degranulation in mast cells.

56 artate receptor (NMDA-R) agonist, leading to calcium influx and downstream cell signaling events and

57 ought transporters involved in mitochondrial calcium influx and efflux have recently been identified.

58 Calcium influx and FM1-43 uptake were found to always be

59 activation of Gq/11-dependent intracellular calcium influx and Gi/o-dependent inhibition of adenylyl

60 y protects against FFA-induced impairment of calcium influx and GSIS in vitro and in vivo but does no

61 d without FFA reproduces the defects in both calcium influx and GSIS, suggesting that upregulation of

62 n-depleted podocytes enhanced TRPC6-mediated calcium influx and induced apoptosis.

63 drenaline on TRPV1 channels was dependent on calcium influx and linked to calcium/calmodulin-dependen

64 Cell death caused by CTX involved calcium influx and mitochondrial damage both in murine C

65 l damage after spinal cord injury depends on calcium influx and mitochondrial permeability transition

66 efects in membrane repair/integrity leads to calcium influx and myofiber necrosis leading to progress

67 or the homeostatic modulation of presynaptic calcium influx and neurotransmitter release.

68 Mechanistically, histones induced profound calcium influx and overload in cultured cardiomyocytes w

69 receptor overstimulation, leading to excess calcium influx and oxidative stress.

70 y expressed in brain and kidney and mediates calcium influx and promotes cell migration.

71 was independent of syntaxin-1, but required calcium influx and protein kinase C (PKC) activity.

72 e control of insulin secretion rate (ISR) by calcium influx and signaling from cytochrome c in islets

73 oda1, a chemical activator of Piezo1, causes calcium influx and subsequent dehydration of RBCs via do

74 prevented D1R-mediated facilitation of NMDAR-calcium influx and subsequent ERK activation.

75 of ATP is independent of calcium influx, but calcium influx and subsequent increase in CBF are depend

76 to depolarize them to voltages necessary for calcium influx and synaptic vesicle fusion.

77 w a tight functional coupling between CaV1.3 calcium influx and the intermediate-conductance KCa3.1 p

78 king to the plasma membrane was secondary to calcium influx and was mediated by its C2A and C2B domai

79 genin3 but requires membrane depolarization, calcium influx, and calcineurin signaling.

80 e (MMP) production (MMPs 1-3), intracellular calcium influx, and cell morphology.

81 al factors to changes in membrane potential, calcium influx, and cell signaling.

82 eek letter for gamma reduces the ACh-induced calcium influx, and depending on their temporal sequence

83 line vesicle release, diminishes presynaptic calcium influx, and diminishes the size of the readily-r

84 ng repetitive activity, enhanced presynaptic calcium influx, and elevated neurotransmitter release.

85 higher channel open probability, induce more calcium influx, and enhance glutamatergic transmission.

86 n between the ER and PM for lipid transport, calcium influx, and ER morphology in mammalian and funga

87 els of NR2B and GluR2, enhanced NMDA-induced calcium influx, and increased miniature excitatory posts

88 ge of axons, increasing blood flow, reducing calcium influx, and inhibiting the accumulation of micro

89 ncreatic islet beta-cell membrane potential, calcium influx, and insulin secretion, and consequently,

90 ormal calcium channel abundance, presynaptic calcium influx, and neurotransmitter release.

91 the release of adenosine triphosphate (ATP), calcium influx, and PKA activation.

92 ia, resulting in loss of membrane potential, calcium influx, and release of glutamate.

93 tead, the effect of HMBA was downstream of a calcium influx, and required the pattern recognition rec

94 polarization of mitochondria, ATP depletion, calcium influx, and the accumulation of ROS, yet cell de

95 s perturbations in firing through changes in calcium influx, and translates this into compensatory ch

96 Retrieval of this pool required large calcium influx, and was inhibited by blockers of calcium

97 occur as a result of excessive intracellular calcium influx, and we have previously shown that angiot

98 toma protein profile of hypophosphorylation, calcium influx, and YY1 proteolysis.

99 naptic activation of NMDARs nor postsynaptic calcium influx are required for its induction.

100 cell loss, result in multiple mechanisms of calcium influx around epithelial wounds.

101 ic homeostasis requires enhanced presynaptic calcium influx as a mechanism to potentiate vesicle rele

102 cell membranes, which would otherwise induce calcium influx as the major mechanism of cytotoxicity ca

103 cci specifically required a sodium-dependent calcium influx, as shown using calcium and sodium transp

104 In a fluorescence-based calcium influx assay, TROX-1 inhibited Ca(V)2.2 channels

105 ctor-induced perinuclear calcium spiking and calcium influx at the root hair tip were blocked.

106 es: intra-nuclear calcium oscillations and a calcium influx at the root hair tip.

107 d that tubulin deacetylation is initiated by calcium influx at the site of injury, and requires prote

108 ion does require membrane depolarization and calcium influx but appears to rely mostly on a distal st

109 in spontaneous neurotransmission depended on calcium influx but did not require activation of voltage

110 d-type NSP4 activated STIM1, resulting in PM calcium influx, but an NSP4 viroporin mutant failed to i

111 ore, apical release of ATP is independent of calcium influx, but calcium influx and subsequent increa

112 Reducing calcium influx by blocking R-type voltage-gated calcium

113 polarizes the cell but paradoxically reduces calcium influx by inactivating voltage-dependent calcium

114 e in cGMP levels, so that cGMP inhibition of calcium influx can limit NO production.

115 , affects calcium entry and small changes in calcium influx can produce large changes in postsynaptic

116 ted transient spine expansion in response to calcium influx caused by NMDA receptor activation.

117 ed presynaptic calcium channel abundance and calcium influx, changes that are independent of the pres

118 tores and activation of plasma membrane (PM) calcium influx channels, ultimately causing a 2- to 4-fo

119 tric pulse (nsEP) exposure generates reduced calcium influx compared to a unipolar (UP) nsEP.

120 These additive effects on calcium influx correlate with the additive effects of mu

121 agent; Gramicidin, eliciting K(+) efflux and calcium influx; dithiocarbamate, a metal ionophore; and

122 Weak calcium influx does not promote closure, but facilitates

123 ain, and phosphorylation results in enhanced calcium influx due to increased channel open probability

124 transiently activated by calcium sparks and calcium influx during action potentials and control the

125 rites of cortical pyramidal neurons regulate calcium influx during backpropagating APs in a distance-

126 of these effects were found, suggesting that calcium influx during pre-depolarizations is required fo

127 g the output of central neurons by providing calcium influx during repetitive inputs.

128 yl)methanone; (CIQ)] enhanced vagal afferent calcium influx during stimulation.

129 present work uses voltage steps to regulate calcium influx during the application of ACh to hair cel

130 ffer in aging neurons balances the increased calcium influx following a small number (<3) action pote

131 hed conditions and 1.8, 0.69, and 1.1 muM by calcium influx for Ca(V)2.1, Ca(V)2.2, and Ca(V)2.3, res

132 anced by channel gating, prevents changes in calcium influx from occurring at the end of the AP and t

133 frequency action potential bursts and alters calcium influx from single action potential stimuli.

134 at in its tetrameric form is responsible for calcium influx from the extracellular environment into t

135 ed cells demonstrated normal glucose-induced calcium influx, further indicating beta cell functionali

136 aptic events occurred earlier as presynaptic calcium influx grew larger.

137 NMDA receptor-dependent calcium influx has been shown to regulate the RAS-ERK pa

138 They elicited calcium influx, hyperalgesia and induced pro-nociceptive

139 mplementary to this, a facilitator of L-type calcium influx impairs retrieval in wild-type mice.

140 gard to their potency to inhibit ATP-induced calcium influx in 1321N1 astrocytoma cells stably transf

141 EG application potentiated capsaicin-induced calcium influx in a subset of sensory neurons.

142 iminating Nox2 ROS production would decrease calcium influx in adult mdx mice and that MEMRI would be

143 -dependent calcium channel (VDCC)-intervened calcium influx in airway epithelial cells, resulting in

144 and guinea pig vagus in vitro, and inhibited calcium influx in airway-specific neurons in vitro.

145 In addition, AYP evoked calcium influx in approximately 1.5% of cultured DRG neu

146 ability to block capsaicin and acid-induced calcium influx in CHO cells expressing human TRPV1.

147 pyridine 4 as an inhibitor of icilin-induced calcium influx in CHO cells expressing recombinant rat T

148 ing pathway was found to inhibit AMPA-evoked calcium influx in cortical neurons and this regulation m

149 Depolarization-induced calcium influx in dorsal root ganglion (DRG) neurons was

150 V1, but not of TRPA1, diminished AYP-induced calcium influx in DRG neurons and the scratching behavio

151 gen species (ROS) production reduced in vivo calcium influx in dystrophic muscle.

152 nce of shear-stress-evoked ionic current and calcium influx in endothelial cells and the ability of e

153 propose that either increase or decrease in calcium influx in excitable cells can be associated with

154 dibenzyl-2-(1H-indol-3-yl)ethanamine, 12) of calcium influx in HEK293 cells.

155 Ss) in GluR2 and NR2B, inhibits NMDA-induced calcium influx in hippocampal neurons, and protects the

156 In addition, we observed an increased calcium influx in KCl-depolarised cells expressing mutat

157 asma membrane calcium channel ORAI1 mediates calcium influx in LECs and activates calmodulin to facil

158 on of p-Src and potentiation of NMDA-induced calcium influx in mouse hippocampal neurons in a dose-de

159 homo-tetramers and their activation mediates calcium influx in oocytes and eggs, which is fundamental

160 SMF stimulation increases the intracellular calcium influx in OPCs as well as the gene expression of

161 6 (TRPC6) channel expression and ATP-induced calcium influx in podocytes of Podo-GC-A KO mice.

162 ese changes were associated with exaggerated calcium influx in presynaptic neurons during high-freque

163 d biochemical studies show that pH regulates calcium influx in proteoliposomes.

164 CD36 regulates membrane calcium influx in response to endoplasmic reticulum (ER)

165 emonstrate participation of CD36 in membrane calcium influx in response to ER stress or purinergic re

166 tion; and (v) infected neurons have impaired calcium influx in response to glutamate.

167 nstrate that keratinocytes rely on TRPV4 for calcium influx in response to histaminergic pruritogens.

168 a and superoxide dismutase 2 levels, reduced calcium influx in response to oxidative stress, and enha

169 However, despite a defect in baseline calcium influx in rim mutants, the homeostatic modulatio

170 Calcium influx in Teffs was quantified using fura-2.

171 ials had larger amplitudes producing greater calcium influx in the distal dendrites of fmr1-/y neuron

172 The increased calcium influx in the mutation prolonged action potentia

173 Low oxygen induces calcium influx in these neurons, and Gucy1b2 and Trpc2 a

174 supporting the importance of TRPC6-mediated calcium influx in this process.

175 tes of TRPA1, activating inward currents and calcium influx in transfected cells and sensory neurons,

176 CIM0216 evoked robust calcium influx in TRPM3-expressing somatosensory neurons

177 synaptic SPHK-1 abundance whereas increasing calcium influx increases SPHK-1 synaptic abundance.

178 ble ratiobetric integrator (CaMPARI) reports calcium influx induced by synaptic and neural activity.

179 ble ratiobetric integrator (CaMPARI) reports calcium influx induced by synaptic and neural activity.

180 mbrane bleb growth, while sodium efflux (and calcium influx) induced by NCX1 in a reverse mode result

181 al activation of TRPV1 by capsaicin leads to calcium influx-induced adaptation of the channel.

182 Calcium influx initiates signaling cascades important fo

183 ergic synapses, while leaving NMDAR-mediated calcium influx intact.

184 s efficacy on axonal damage, blood flow, and calcium influx into axons in a mouse SCI model.

185 se cells, and a role for actin in regulating calcium influx into cells has been suggested.

186 -bistrifluoromethyl pyrazole, which inhibits calcium influx into cells.

187 results in a location-dependent increase in calcium influx into dendrites and spines during backprop

188 Ucn 2 decreased calcium influx into freshly isolated dystrophic muscles.

189 ission through modulation of low-level tonic calcium influx into presynaptic axon terminals.

190 Studies on calcium influx into RUB cells show that in the presence

191 negative feedback loop due to inhibition of calcium influx into the cell by cyclic guanosine monopho

192 Together, these data suggest that, following calcium influx into the cell, pro-IL-1beta interacts wit

193 Glutathione depletion and calcium influx into the cytoplasm are two hallmarks of a

194 with additional possibilities for regulating calcium influx into the cytosol.

195 We show that, on recognition of targets, calcium influx into the lymphocyte led to perforin exocy

196 properties that can influence the amount of calcium influx into the spine.

197 ce of anti-DPP, there was a 40% reduction of calcium influx into these cells.

198 P3CA, PPP3CB, PPP3R1, and NFATC3 expression; calcium influx; intracellular Ca2+ concentration; and ca

199 We hypothesized here that Ang II-mediated calcium influx is aggravated in the podocytes under the

200 nodule development; we wanted to test if the calcium influx is associated with infection.

201 Surprisingly, this rapid calcium influx is blocked by the N-type calcium channel

202 otentials (effective RRP), we find that when calcium influx is changed by altering the external calci

203 k characterized by high-frequency firing and calcium influx is highly suited to modify synaptic effic

204 that activation of the pathway involving the calcium influx is important for efficient infection.

205 y reports voltage and calcium indicated that calcium influx is induced by voltage depolarizations, si

206 ctivate multiple calcium channels in the PM, calcium influx is predicated on NSP4 viroporin-mediated

207 Excessive calcium influx is thought to initiate the pathogenic cas

208 Although most presynaptic calcium influx is through N-type and P/Q-type calcium ch

209 f presynaptic action potentials that delimit calcium influx, large pools of rapidly mobilized vesicle

210 d mouse sensory neurons revealed that axonal calcium influx late in the degeneration process regulate

211 appears to have been a loss of diversity in calcium-influx mechanisms at the plasma membrane.

212 fied hypoxic impairment of islet response by calcium influx, mitochondrial potentials, and insulin se

213 ht controls, p < 0.05), and also accelerated calcium influx (n = 9) and enhanced nitric oxide product

214 ds on STIM2-mediated neuronal store-operated calcium influx (nSOC) and continuous activity of Ca(2+)/

215 In contrast, a second phase of calcium influx occurring minutes before fragmentation sp

216 After ACh-GABA pairing the calcium influx of a subsequent excitatory stimulus is in

217 anization of input fibres does not depend on calcium influx or dynamics.

218 Whether this calcium signal is generated by calcium influx or requires calcium-induced calcium relea

219 detected in the imaged neurons as increased calcium influx or synaptic release in response to the co

220 Pharmacological blockade of NMDA-R, calcium influx, or calpain activity abolished SSC and gl

221 re the main components of a widely conserved Calcium influx pathway known as store-operated calcium e

222 r imaging of axonal dieback, blood flow, and calcium influx post-injury.

223 of axons, increased blood flow, and reduced calcium influx post-injury.

224 n rim mutants, the homeostatic modulation of calcium influx proceeds normally.

225 ow that the reduction is due to an effect on calcium influx rather than calcium release from intracel

226 terminals reveals that blocking presynaptic calcium influx reduces synaptic SPHK-1 abundance whereas

227 Early electrical activity and calcium influx regulate crucial aspects of neuronal deve

228 These findings indicate that calcium influx regulates the RRP size along with p, whic

229 ut the underlying mechanisms responsible for calcium influx remain poorly understood.

230 Specifically, the local calcium influx responsible for vesicular release and sho

231 It might block the excessive calcium influx resulting from the aberrant expression of

232 rentiation that is known to depend on L-type calcium influx, Rho-activation, and actin polymerization

233 ing, resulting in phosphorylation of PLC-g1, calcium influx, ROS generation, upregulation of FASL, an

234 ive disorders, is characterized by excessive calcium influx selectively through NMDARs.

235 an-Iav complexes that, by promoting cellular calcium influx, silence the stretch receptor cells.

236 of the stimulation train, which induces more calcium influx, slows down endocytosis; and several stud

237 ive target cell engagement, as determined by calcium influx studies.

238 s the activation of neuronal NMDA receptors, calcium influx, subsequent ATP release, and microglial r

239 s examined by treating cells with ionomycin (calcium influx), thapsgargin (endoplasmic reticulum [ER]

240 as blockers of the L-type voltage-dependent calcium influx that activates the sAHP, rescue retrieval

241 , high-voltage pulses in tumors enables high calcium influxes that trigger cell death.

242 While the trans isomer primarily engages calcium influx, the cis isomer favors cAMP generation.

243 mice NLF significantly limits mitochondrial calcium influx, the event associated with protection of

244 Within seconds of calcium influx, the formin INF2 stimulates filament poly

245 Downstream of this calcium influx there was protease activation and spatial

246 ximum intraburst firing rates require axonal calcium influx through Dmca1D channels, likely to enhanc

247 s regulate action potential firing and shape calcium influx through feedback regulation in mature neu

248 Proton-evoked membrane currents and calcium influx through hTRPA1 occurred at physiological

249 is regulated at the transcriptional level by calcium influx through L-VGCCs and inhibits dendritic ar

250 We then provide evidence that calcium influx through synaptic CaV2.1 channels and subs

251 Pore altering mutations that prevent calcium influx through the channel prevented significant

252 Calcium influx through the L-type Ca(2+) channel is crit

253 an important partner in regulating immediate calcium influx through the surface membrane readily acco

254 Calcium influx through the voltage-dependent L-type calc

255 depolarization during action potentials, and calcium influx through them is the key second messenger

256 that the effective RRP size is dependent on calcium influx through VGCCs.

257 This limits calcium influx through voltage-dependent calcium channel

258 tion that extends the contribution of CaV1.3 calcium influx to a time frame well beyond a brief input

259 isting CaV3.2 channels, and can induce local calcium influx to control NMDA transmission strength in

260 synaptotagmin-1 (SYT) is required to couple calcium influx to the membrane fusion machinery.

261 ally excitable cells harness voltage-coupled calcium influx to transmit intracellular signals, typica

262 ats, and increased response to Ang II; total calcium influx triggered by Ang II application was also

263 At the cellular level, calcium influx triggered by beta-alanine is also unchang

264 Strong calcium influx triggers dynamin-mediated closure.

265 Presynaptic calcium influx triggers synaptic vesicle (SV) exocytosis

266 entrations) inhibited LPS (50 ng/ml)-induced calcium influx, tumor necrosis factor-alpha, and nitric

267 possibly leading to increased intracellular calcium influx, underlies the pathogenesis of the TRPV4-

268 Under these conditions, e-LXA4 decreased the calcium influx versus that observed in LPS-stimulated BM

269 channel (CatSper), and its removal leads to calcium influx via CatSper and ensures sperm activation.

270 ich led to a reduction in activity-dependent calcium influx via Cav channels.

271 genes and proteins, albumin endocytosis, and calcium influx via podocyte-specific transient receptor

272 ls induced reactive oxygen species-dependent calcium influx via the TRPM2 channel and that macrophage

273 the kinase upstream of ERK, suggesting that calcium influx via TRPV4 in keratinocytes leads to ERK-p

274 ecifically, water influx through AQP4 drives calcium influx via TRPV4 in the glial end foot, which re

275 The emerging model is that calcium influx via voltage-dependent calcium channels at

276 ions (Na, Mg) increased with Ni exposure and calcium influx was depressed.

277 The calcium influx was even further reduced if the N-linked

278 Depletion-evoked calcium influx was initiated at the Muller end-foot and

279 Calcium influx was measured by using Fluo-4 intensity.

280 When calcium influx was minimized during pre-depolarization,

281 Calcium influx was observed when as few as 2000 oligomer

282 Unexpectedly, glucose-stimulated calcium influx was only slightly reduced in low glucose-

283 Calcium influx was prevented by the presence in the pipe

284 hanistic experiments in vitro indicated that calcium influx was similar in fibroblasts and cancer cel

285 When calcium influx was terminated at positive membrane poten

286 at evoked an inward depolarizing current and calcium influx, whereas other analogs did not exhibit th

287 least partly on an inhibition of presynaptic calcium influx, which controls glutamate release.

288 postsynaptic currents and, more relevant, to calcium influx, which could be involved in the modulatio

289 been unclear, but we found that GABA blocked calcium influx, which is a key activation signal.

290 gnificantly reduced GHS-R1a agonist-mediated calcium influx, which was completely restored following

291 Light elicited calcium influx, which was mitigated by SFZ.

292 prevent spontaneous fusion in the absence of calcium influx, while at the same time facilitating rele

293 -AP5) significantly inhibited vagal terminal calcium influx, while the excitatory amino acid reuptake

294 ed by measuring ear thickness and histology, calcium influx with Fura-2, phosphorylation and expressi

295 to the calcium channel so as to synchronize calcium influx with membrane fusion.

296 calcium buffering with EGTA-AM or decreasing calcium influx with omega-agatoxin IVA decreased the amo

297 hat MCTP functions downstream of presynaptic calcium influx with separable activities to stabilize ba

298 onist, ifenprodil, selectively reduced vagal calcium influx with stimulation compared to the time con

299 tity of specific channel proteins regulating calcium influx within the lens is not completely underst

300 cetyl group greatly reduced the induction of calcium influx without affecting calcium spiking.