ライフサイエンスコーパス: calcium release

1 found that the H2R induces Galphaq-mediated calcium release.

2 but no effect on intracellular RyR2-mediated calcium release.

3 ge changes and then triggering intracellular calcium release.

4 n, which in turn results in another abnormal calcium release.

5 to the nucleus specifically after lysosomal calcium release.

6 ,4,5-trisphosphate-dependent intra-acrosomal calcium release.

7 tic calcium release mediated by enhanced RyR calcium release.

8 es to phospholipase C-mediated intracellular calcium release.

9 lation and enhanced 5-HT2A receptor-mediated calcium release.

10 f IP3 at concentrations sufficient to induce calcium release.

11 bout the mechanism coupling NAADP binding to calcium release.

12 (3)RII levels and therefore pro-hypertrophic calcium release.

13 ryanodine receptor by way of calcium-induced calcium release.

14 ion of PLCgamma1 and increased intracellular calcium release.

15 sitol 1,4,5-trisphosphate receptor-dependent calcium release.

16 ation, or by ionomycin-induced intracellular calcium release.

17 ven in the presence of direct stimulators of calcium release.

18 release profile and the rate of spontaneous calcium release.

19 ex is required specifically for Fas-mediated calcium release.

20 estospongin C, an inhibitor of IP3R-mediated calcium release.

21 o-pore channel-mediated triggering of global calcium release.

22 agy by activating the ryanodine receptor and calcium release.

23 is mediated by ryanodine receptor-dependent calcium release.

24 s released by the process of calcium-induced calcium release.

25 ontent and its more pronounced decline after calcium release.

26 tokine-mediated suppression of functional ER calcium release.

27 -RyRs increases the incidence of spontaneous calcium release.

28 loma cells accompanied by apoptosis-inducing calcium release.

29 n of TMTC1 or TMTC2 increased the stimulated calcium released.

30 endothelial NO synthase is activated 1), via calcium release, 2), via phosphorylation reactions, and

31 nship between abnormal TATS and asynchronous calcium release, a major determinant of cardiac contract

32 Store-operated calcium entry (SOCE) by calcium release activated calcium (CRAC) channels consti

33 ed to wild-type cells as a result of reduced calcium release activated calcium currents, and independ

34 interaction molecule 1) clustering and CRAC (calcium release activated calcium) channel activation.

35 forms a highly calcium-selective pore of the calcium release activated channel, and alpha-SNAP is nec

36 ulum, followed by opening of plasma-membrane calcium-release activated calcium (CRAC) channels.

37 membrane protein Orai forms the pore of the calcium release-activated calcium (CRAC) channel and gen

38 Remarkably, BTP2, a small-molecule calcium release-activated calcium (CRAC) channel blocker

39 ORAI1 is the pore-forming subunit of the calcium release-activated calcium (CRAC) channel, a stor

40 rystal structure of Orai, the pore unit of a calcium release-activated calcium (CRAC) channel, is use

41 ia activates AMPK by ROS-mediated opening of calcium release-activated calcium (CRAC) channels.

42 illatory to a sustained elevated pattern via calcium release-activated calcium (CRAC)-mediated capaci

43 traps Orai1 in the PM through binding of its calcium release-activated calcium activation domain.

44 The two key components of the store-operated calcium release-activated calcium channel are the Ca(2+)

45 odulatory drug inhibiting the store-operated calcium release-activated calcium channel of lymphocytes

46 The calcium release-activated calcium channel Orai regulates

47 ignal mediator, ORAI1, a pore subunit of the calcium release-activated calcium channel, was identifie

48 In addition to calcium release-activated calcium channel/ORAI calcium c

49 vation of engineered chemokine receptors and calcium release-activated calcium channels.

50 tromal interaction molecule (STIM) 1 and the calcium release-activated calcium modulator (ORAI) 1-med

51 The stromal interaction molecule (STIM)-ORAI calcium release-activated calcium modulator (ORAI) pathw

52 phocytes express not only cell membrane ORAI calcium release-activated calcium modulator 1 but also v

53 lation of stromal interaction molecule 1 and calcium release-activated calcium modulator 1 expression

54 nts, such as stromal interaction molecule 1, calcium release-activated calcium modulator 1, and trans

55 CRAC (Calcium Release-Activated Calcium) channels represent th

56 hly Ca(2+)-selective channels known as CRAC (calcium release-activated calcium) channels.

57 ew studies have recorded STIM2-induced CRAC (calcium release-activated calcium) currents.

58 y LFA-1 facilitates the cooperation with the calcium release-activated channel Orai1 in directing loc

59 the activation of plasma membrane-associated calcium release-activated channels.

60 ained by Ca(2+) entry through store-operated calcium-release-activated calcium (CRAC) channels.

61 0% (P<0.001, n=18), and promoted spontaneous calcium release activity (n=14, P<0.013) in human cardia

62 ased Ca2+ alternans and promoted spontaneous calcium release activity in human cardiac myocytes deriv

63 rane calcium gradient is established can the calcium-release activity of holo-BsYetJ occur and be med

64 Additionally, the calcium release allows the N-lobe to rotate relative to

65 Disruption of intracellular calcium release also prevented DIR.

66 nation of specially developed cell lines and calcium release analysis hardware, has created a new and

67 e- or inositol 1,4,5-trisphosphate-dependent calcium release and abolished when both lysosomal and en

68 lacement of CGB decreases InsP(3)R-dependent calcium release and alters normal signaling patterns.

69 ulations based on a model of calcium-induced calcium release and cell-to-cell diffusion through gap j

70 entation has been shown to increase myofibre calcium release and force production in mouse skeletal m

71 s provide insight into regulation of cardiac calcium release and how alterations to this process may

72 to impaired Pitx2 by preventing spontaneous calcium release and increasing wavelength.

73 tment of HSG cells resulted in intracellular calcium release and induction of endocytosis at levels s

74 ct independently of beta-catenin to modulate calcium release and influence cell polarity.

75 g that H(2)O(2) accumulation is dependent on calcium release and Krebs cycle activity.

76 mutation decreases sensitivity to activated calcium release and myoplasmic calcium levels, subsequen

77 indicating that NO synthesis is dependent on calcium release and occurs in organelles.

78 evoke redistribution, even though it caused calcium release and Orai1-mediated calcium entry in the

79 PKA can drive internal calcium release and promote calcium flow through NMDAR a

80 n cysteine residues on intralumenal loops of calcium release and reuptake channels have been implicat

81 ake channels have been implicated in altered calcium release and reuptake.

82 fects and acting to promote effects, such as calcium release and stress signaling, via intracellular

83 pathway that induces local intracytoplasmic calcium release and subsequent damage in neurons.

84 ed [Ca(2+)]cyt spikes were primarily from ER calcium release and were attenuated by inhibiting the st

85 ering membrane depolarization, intracellular calcium release, and actomyosin contraction.

86 tol triphosphate accumulation, intracellular calcium release, and directed cell migration.

87 t duration, increased incidence of diastolic calcium release, and ectopic contractility.

88 ent cytosolic and mitochondrial pH decrease, calcium release, and phosphorylation of stress signaling

89 ng events (eg, Akt activation, intracellular calcium release, and Ras-associated protein 1 [Rap1] exp

90 Calcium release at 2, 3, and 12 h was inhibited by 2-(4-

91 eractions between synaptically and ER-evoked calcium release at glutamatergic synapses in young AD tr

92 The grafts exhibit contractile and calcium release behavior, characteristic of functional m

93 e reduction of ryanodine receptor 1 mediated calcium release but, since knocking out genes in animal

94 7,8-diol (SKF83959), found no stimulation of calcium release, but it did find a broad range of cross-

95 osed role of calsequestrin in termination of calcium release by conformationally inducing closure of

96 Lysosomal calcium release by TRPML1 promotes calcium transfer to m

97 lts, polymer treatment reduced the amount of calcium released by 27% to 30% in comparison with the un

98 We demonstrated that mitochondrial calcium released by voltage-dependent anion channel 1 (V

99 F-TrkA-dependent signaling events, including calcium release, calcineurin activation and phosphorylat

100 alcium levels upon addition to cell culture, calcium release can be determined in these cell lines up

101 in the SR lumen after depolarization-induced calcium release cause the dissociation of JP45 from CASQ

102 skeletal muscle sarcoplasmic reticulum (SR) calcium release channel (ryanodine receptor, RyR1 isofor

103 e mammalian ryanodine receptor intracellular calcium release channel (RyR) with high (fM) potency and

104 um channel directly activates opening of the calcium release channel (RyR1) in the sarcoplasmic retic

105 Ca2+ leak via the cardiac ryanodine receptor/calcium release channel (RyR2) is thought to play a role

106 le, including the cardiac ryanodine receptor/calcium release channel (RyR2) required for muscle contr

107 The type 2 ryanodine receptor/calcium release channel (RyR2), required for excitation-

108 r (ITPR3) is the most abundant intracellular calcium release channel in cholangiocytes.

109 risphosphate receptor (ITPR2), the principle calcium release channel in hepatocytes.

110 he podocyte type 2 ryanodine receptor (RyR2)/calcium release channel on the ER was phosphorylated, re

111 CPVT mutations alter protein function, RyR2 calcium release channel regulation, and cellular calcium

112 The skeletal muscle calcium release channel RyR1 is activated by Ca(2+)-free

113 e of CPVT: RYR2 (encoding ryanodine receptor calcium release channel), CASQ2 (encoding cardiac calseq

114 hionine oxidation on CaM's regulation of the calcium release channel, ryanodine receptor (RyR).

115 yanodine receptor (RyR), a large endoplasmic calcium release channel.

116 ich triggers proteasomal degradation of this calcium release channel.

117 of the major cardiac sarcoplasmic reticulum calcium release channel/ryanodine receptor (RyR2), at Se

118 antial reduction in the expression levels of calcium release channels (ryanodine receptors, RyR2) in

119 pilepsy, is a diastolic inhibitor of cardiac calcium release channels [cardiac ryanodine receptor 2 (

120 receptors (RyRs), a family of intracellular calcium release channels essential for many cellular pro

121 d as a novel family of endolysosome-targeted calcium release channels gated by nicotinic acid adenine

122 ble progress has been made in characterizing calcium release channels in the nuclear membrane, very l

123 rons by stabilizing ryanodine receptor (RyR) calcium release channels in the open configuration, whic

124 ceptors (RyRs) form a class of intracellular calcium release channels in various excitable tissues an

125 Ryanodine receptors (RyRs) form calcium release channels located in the membranes of the

126 Ryanodine receptors (Ryrs) are a family of calcium release channels on intracellular stores.

127 Ryanodine receptor (RyR) calcium release channels showed lower sensitivity to caf

128 ine receptor types 1 (RyR1) and 2 (RyR2) are calcium release channels that are highly enriched in ske

129 P2XRs regulate vacuole activity by acting as calcium release channels, activated by translocation of

130 protein that stabilizes the closed state of calcium release channels, i.e. the ryanodine receptors.

131 Ryanodine receptors (RyR) are calcium release channels, playing a major role in the re

132 el, and the intracellular ryanodine receptor calcium release channels.

133 e receptors are homotetrameric intracellular calcium release channels.

134 and functions (phagocytosis, degranulation, calcium release, chemotaxis, and reactive oxygen species

135 essed for receptor function, using assays of calcium release, chemotaxis, receptor endocytosis, and l

136 e regulation of regenerative calcium-induced calcium release (CICR) during Ca(2+) spark evolution rem

137 ggesting that LMO4 regulates calcium-induced calcium release (CICR) in central neurons.

138 Stable calcium-induced calcium release (CICR) is critical for maintaining norma

139 y calcium influx or requires calcium-induced calcium release (CICR) is not yet known.

140 xtension of the smooth ER, a calcium-induced calcium release (CICR) is triggered at the base of the s

141 minished by the inhibitor of calcium-induced calcium release (CICR), dantrolene.

142 In skeletal muscle, proteins of the calcium release complex responsible for the excitation-c

143 k-Y130E were deficient in antigen-stimulated calcium release, degranulation, and production of some c

144 cific for either MAPK/ERK phosphorylation or calcium release demonstrated that the two pathways conve

145 The effect of N-CGB on calcium release depended upon endogenous levels of cellu

146 ar calcium storage compartment, facilitating calcium-release-dependent cellular processes.

147 nd on a beat-to-beat basis and mitochondrial calcium release depends on mNCE activity and mitochondri

148 Biochemically, we show that Spry3 represses calcium release downstream of BDNF signalling.

149 Blockade of lysosomal calcium release due to lysosomal lipid accumulation has

150 roperties, elevated NOX2 expression, altered calcium release dynamics, how NADPH oxidase 2 is activat

151 Moreover, reduction of mitochondrial calcium release, either by shRNA-mediated VDAC1 silencin

152 r GCaMP in the spermatheca exhibit premature calcium release, elevated calcium levels, and disrupted

153 amic copper redistributions are dependent on calcium release, establishing a link between mobile copp

154 Spontaneous sub-cellular calcium release events (SCRE) are conjectured to promote

155 ayed Ca(2+) transients, frequent spontaneous calcium release events and increased susceptibility to p

156 demonstrated increased frequency of abnormal calcium release events, which was suppressed by a cell-p

157 Increasing HP causes calcium release from a ryanodine-sensitive cytoplasmic s

158 that sphingosine is a positive regulator of calcium release from acidic stores and that understandin

159 er hypothesis for NAADP action proposes that calcium release from acidic stores subsequently acts to

160 ne Dinucleotide Phosphate (NAADP) stimulates calcium release from acidic stores such as lysosomes and

161 ged Sph leads to a significant and transient calcium release from acidic stores that is independent o

162 ium storage, 1,25(OH)(2)D not only increases calcium release from bone, but also inhibits calcium inc

163 lation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leadi

164 ents showed that L-type calcium channels and calcium release from internal stores are both required f

165 showed that the potentiation of RyR-mediated calcium release from internal stores by caffeine was abs

166 ibition of voltage-gated calcium channels or calcium release from internal stores reduces regenerativ

167 ists include a significant contribution from calcium release from internal stores.

168 sphate (NAADP) is a messenger that regulates calcium release from intracellular acidic stores.

169 Cholinergic inhibitory responses depend on calcium release from intracellular calcium stores, and r

170 o block or enhance CICR to determine whether calcium release from intracellular stores affected actio

171 Interestingly, BMP-2 induced calcium release from intracellular stores and increased

172 ular communication through gap junctions and calcium release from intracellular stores as mediators o

173 lso produces vasomotor responses by inducing calcium release from intracellular stores through its pr

174 ) activates signaling cascades, resulting in calcium release from intracellular stores, ERK1/2 activa

175 beta-cell BDNF-TrkB.T1 signaling triggers calcium release from intracellular stores, increasing gl

176 ults demonstrate that, in addition to gating calcium release from intracellular stores, mAChR activat

177 ibition of N- or P/Q-type VDCCs, or block of calcium release from intracellular stores.

178 e to an effect on calcium influx rather than calcium release from intracellular stores.

179 ospholipase C gamma(1), critical signals for calcium release from intracellular stores.

180 Calcium release from liposome-HGN can be spatially patte

181 1a-mediated inositol phosphate formation and calcium release from mouse neurons in a PKC-dependent ma

182 erved function of AIP proteins is to inhibit calcium release from ryanodine receptors.

183 Abnormal calcium release from sarcoplasmic reticulum (SR) is cons

184 aled a unique receptor-mediated mechanism of calcium release from SGs that involves SG store-operated

185 ening on SG membranes as a potential mode of calcium release from SGs that may serve to raise local c

186 either L-type calcium channel activation or calcium release from stores is sufficient to permit pote

187 Here we show that calcium release from the axonal endoplasmic reticulum (E

188 gnal-induced nuclear actin responses require calcium release from the endoplasmic reticulum (ER) targ

189 helial hyperplasia via apoptosis mediated by calcium release from the endoplasmic reticulum (ER), but

190 Induction of calcium release from the endoplasmic reticulum also lead

191 istically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrop

192 yR2-R4496C mutant HEK-293 cell line in which calcium release from the endoplasmic reticulum through t

193 We find here that localized calcium release from the endoplasmic reticulum via ryano

194 where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed

195 ed CD36 function in FA uptake and FA-induced calcium release from the endoplasmic reticulum, supporti

196 caused an increase in the InsP(3)-dependent calcium release from the endoplasmic reticulum.

197 as indicated by reduced RyR agonist-induced calcium release from the ER and RyR-mediated synaptic re

198 n induces endoplasmic reticulum (ER) stress, calcium release from the ER and subsequent uptake of cal

199 m overload in SOD1G93A astrocytes and excess calcium release from the ER during ATP stimulation.

200 d that purinergic stimulation induces excess calcium release from the ER stores in SOD1G93A astrocyte

201 FasL stimulation and found that LFG inhibits calcium release from the ER, a process that correlates w

202 Once liberated, ACh acts to trigger calcium release from the internal store in endothelial c

203 o serve as a countercurrent mechanism during calcium release from the nuclear envelope.

204 ias are caused by unregulated 'pathological' calcium release from the sarcoplasmic reticulum (SR), th

205 PKARIalpha was sufficient to prevent global calcium release from the sarcoplasmic reticulum in LV my

206 macromolecular complex devoted to control of calcium release from the sarcoplasmic reticulum.

207 m acidic stores subsequently acts to enhance calcium release from the SR.

208 oponin complex, CK-2017357 slows the rate of calcium release from troponin C and sensitizes muscle to

209 ner mechanistically dependent upon apoptotic calcium release from voltage-gated calcium channels.

210 Luminal calcium released from secretory organelles has been sugg

211 either TMTC1 or TMTC2 caused a reduction of calcium released from the ER following stimulation, wher

212 ion is roughly proportional to the amount of calcium released from the Sarcoplasmic Reticulum (SR) du

213 The ectopic calcium released from these receptors induces pro-hypert

214 Our findings suggest that calcium released from TPCs is involved in Tat endolysoso

215 tudy we examined the causal role of abnormal calcium releases from the sarcoplasmic reticulum in prod

216 ibrillar mitochondria-directly exposed to SR calcium release-from aged mice had increased calcium con

217 > 10(-4) mol/g of dust, the amount of P (and calcium) released has a direct proportionality to the am

218 esent, mutations in six genes involved in SR calcium release have been identified as the genetic caus

219 assessed by (a) inhibition of intracellular calcium release (IC(50) 10 nM) induced in human monocyte

220 proaches, we demonstrated that IP(3)-induced calcium release (IICR) initiated the hypertrophy-associa

221 cium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stres

222 ring inhibition of UTP-induced intracellular calcium release in 1321N1 astrocytoma cells stably trans

223 al slices, we show that increased RyR-evoked calcium release in 3xTg-AD mice "normalizes" an altered

224 s this question, sarcoplasmic reticulum (SR) calcium release in a mouse strain with a naturally occur

225 imaging of zebrafish embryos shows defective calcium release in bin1 morphants, linking the presence

226 -1-79) potentiated 5-HT-evoked intracellular calcium release in cells stably expressing the human 5-H

227 Refractoriness of calcium release in heart cells is altered in several dis

228 Calcium release in HF myocytes was restricted to regions

229 ty of SDF1-ELP, as measured by intracellular calcium release in HL60 cells was dose dependent, and al

230 We examined refractoriness of calcium release in mouse ventricular myocytes and invest

231 blocked the increased incidence of diastolic calcium release in mutant cells.

232 t amplitude variation in G-protein-activated calcium release in RAW264.7 macrophages is generally ext

233 exacerbated PLC signaling and intracellular calcium release in response to either glutamate or dopam

234 tract, and fail to undergo calcium-dependent calcium release in response to electrical stimulation or

235 y capacity, protein kinase C expression, and calcium release in response to PMA and CF pathogens.

236 lve for the equilibrium open probability for calcium release in the model.

237 Calcium transient duration and diastolic calcium release in the mutant myocytes were tetrodotoxin

238 inity binding of PSC-RANTES, analog-mediated calcium release (in desensitization assays), and analog-

239 We further show that endoplasmic reticulum calcium release-induced store-operated calcium entry con

240 In addition, ER calcium release induces elevated ATP release from SOD1G9

241 We found that refractoriness of calcium release is abbreviated by stimulation of the 'fi

242 vated chloride conductances by intracellular calcium release is the key factor underlying spontaneous

243 emonstrated that ATP dependent intracellular calcium release leads to an increase of nearly 100% in o

244 Specifically, abnormal calcium release leads to electrical activation, which in

245 potent calcium messenger, is able to trigger calcium release, likely through two-pore channels (TPCs)

246 ffects that are dependent upon the apoptotic calcium release machinery.

247 T temperature by sensitizing the TRH-PLC-IP3-calcium release mechanism.

248 supported by a ROS-assisted calcium-induced calcium-release mechanism intimately involving ROS produ

249 a Ca(2+) diffusion-dominated calcium-induced calcium-release mechanism is insufficient to explain the

250 uated their ability to inhibit intracellular calcium release mediated by angiotensin II receptor type

251 the augmented synaptically evoked dendritic calcium release mediated by enhanced RyR calcium release

252 Calcium release mediated by IP3Rs influences many signal

253 dramatically affect calcium homeostasis and calcium release mediated through the ryanodine receptor

254 ternal organelles, specialized intracellular calcium release membranes, come into close apposition wi

255 s to form dyads within which calcium-induced-calcium-release occurs.

256 BAPTA chelation, and recruits intracellular calcium release on its way to activation of phosphatase

257 Inhibition of intracellular calcium release or protein kinase C delta, both of which

258 he results were corroborated by analyses for calcium release or uptake, tartrate-resistant acid phosp

259 hen both lysosomal and endoplasmic reticulum calcium release pathways were blocked.

260 content and sarcoplasmic reticulum-mediated calcium release, preserving cardiomyocyte contraction af

261 f calcium is inherent in the calcium-induced calcium release process.

262 the effect of changing CSQ expression on the calcium release profile and the rate of spontaneous calc

263 at CAPN3 knockout muscles exhibit attenuated calcium release, reduced calmodulin kinase (CaMKII) sign

264 ms that are responsible for the pathological calcium release, regarding the tissue origin of the arrh

265 o indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying caus

266 This photo-induced Sph-driven calcium release requires the two-pore channel 1 (TPC1) r

267 ma 2 (AIM2), which led to higher cytoplasmic calcium release responsible for calpain activation under

268 Calcium influx after ER calcium release resulted in phosphorylation of cPLA(2) a

269 Lastly, we show that ER calcium release resulting from barrier perturbation trig

270 al duration, Ca2+ alternans, and spontaneous calcium release (SCR) incidence were determined.

271 the atria from mice predisposed to abnormal calcium releases secondary to the absence of calsequestr

272 feedforward cycle between the increased RyR calcium release seen in presymptomatic AD mice and aberr

273 of luminal ATP translocation and ATP-evoked calcium release share common pharmacology, suggesting th

274 ts ability to inhibit store-overload-induced calcium release (SOICR) through the RyR2 channel.

275 Cmpt mice exhibited a faster decline in calcium release, suggesting a compromised ability to ref

276 3a, a guidance cue that does not activate ER-calcium release, suggesting multiple functions of STIM1

277 rate and increases the critical SR level for calcium release termination.

278 e directly suppresses sarcoplasmic reticulum calcium release-the cellular mechanism responsible for t

279 behaviour that is modulated by intracellular calcium release through inositol 1,4,5-trisphosphate rec

280 ium activity during axophilic migration, and calcium release through IP3 receptors was found to stimu

281 Herein we report that proper lysosomal calcium release through the calcium channel TRPML1 is re

282 acutely couples changes in pO(2) to altered calcium release through the ryanodine receptor-Ca(2+)-re

283 InsP(3)-mediated calcium release through the type 2 inositol 1,4,5-trisph

284 HSV triggers intracellular calcium release to promote viral entry.

285 s and were proposed to mediate endolysosomal calcium release triggered by the second messenger, nicot

286 fects of IVIg on several parameters, such as calcium release, tyrosine phosphorylation, BCR aggregati

287 vealed a 36% reduction in the number/area of calcium release units accompanied by a 2.5-fold increase

288 ) patients and demonstrate a greatly reduced calcium release upon Sph uncaging.

289 owth behaviors is due to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases

290 ured from females, significantly potentiated calcium release via ryanodine receptors induced by caffe

291 s Akt phosphorylation, inhibited HSV-induced calcium release, viral entry, and plaque formation follo

292 neurons expressing actin-GFP or Lifeact-RFP, calcium release was found to stimulate leading process a

293 Although the voltage dependence of SR calcium release was not statistically different between

294 duration stimulus or a diastolic spontaneous calcium release, we observed that the stimulus needed wa

295 litude and fractional sarcoplasmic reticulum calcium release were larger and action potential and QTc

296 is reversed upon normalization of RyR-evoked calcium release with chronic dantrolene treatment.

297 iant, we show that 5-HT evokes intracellular calcium release with decreased potency and peak response

298 sted selectively inhibited histamine-induced calcium release with the best being chlorprothixene (IC(

299 y inhibiting inositol trisphosphate-mediated calcium release with Xestospongin C (XeC).

300 Moreover, caffeine-induced calcium release yielded no difference between AAA/DDD an