ライフサイエンスコーパス: Ca2 release

1 stained effects of tetracaine on spontaneous Ca2+ release.

2 quence also activate PAR2, often measured by Ca2+ release.

3 for the first time, during a single event of Ca2+ release.

4 fibres to measure SOCE during intracellular Ca2+ release.

5 evokes a larger sarcoplasmic reticulum (SR) Ca2+ release.

6 lining [Ca2+]SR in the dynamic shutoff of SR Ca2+ release.

7 tivation, and inositol triphosphate-mediated Ca2+ release.

8 k loops and drives circadian oscillations of Ca2+ release.

9 its effect is independent of store-dependent Ca2+ release.

10 myocytes and are activated on Ca2+ -induced Ca2+ release.

11 V(m), reduced i(Ca) must explain reduced SR Ca2+ release.

12 badan), and c), effects of "a" and "b" on SR Ca2+ release.

13 e resembling CaMBP-badan/Ca-CaM) and induced Ca2+ release.

14 ded upon stimulation of prolonged, cell-wide Ca2+ release.

15 esembling CaMBP-badan/apo-CaM) and inhibited Ca2+ release.

16 ingle InsP3R channel can account for quantal Ca2+ release.

17 , is thought to mediate the majority of this Ca2+ release.

18 in close proximity to sites of RyR-mediated Ca2+ release.

19 ogical and pathophysiological roles in ER/SR Ca2+ release.

20 monomers and inhibits sarcoplasmic reticulum Ca2+ release.

21 F/p.V1316M acts directly on or downstream of Ca2+ release.

22 ease terminates and increased the fractional Ca2+ release.

23 ociated RyR2 mutations on the termination of Ca2+ release.

24 VEGF-mediated VP by regulating intracellular Ca2+ release.

25 he maximal Ca2+ conductance (gCa) nor the SR Ca2+ release.

26 is essential for efficient triggering of SR Ca2+ release.

27 + signalling via the process of Ca2+-induced Ca2+ release.

28 s, with higher [Ca2+]SR before the larger SR Ca2+ releases.

29 shortening, +/-dL/dt, sarcoplasmic reticulum Ca2+ release, 45Ca uptake, and intracellular Ca2+ decay,

30 cretion to transcription, and is mediated by Ca2+-release activated Ca2+ (I(crac)) channels and store

31 essential for store-operated Ca2+ influx and Ca2+ release-activated Ca2+ (CRAC) channel activity in D

32 Loss-of-function mutations in the Ca2+ release-activated Ca2+ (CRAC) channel genes ORAI1 a

33 amel cells might be mediated by SOCE and the Ca2+ release-activated Ca2+ (CRAC) channel, the prototyp

34 nt phospholipase A2 (iPLA2) in activation of Ca2+ release-activated Ca2+ (CRAC) channels and store-op

35 Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca

36 sustained Ca2+ entry through store-operated Ca2+ release-activated Ca2+ (CRAC) channels, an essentia

37 oughly studied of these conductances are the Ca2+ release-activated Ca2+ (CRAC) channels, and recent

38 of immune cells triggers Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) channels, promoting t

39 by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels.

40 diating store-operated Ca2+ entry (SOCE) and Ca2+ release-activated Ca2+ (CRAC) currents.

41 man homologue Orai1 are pore subunits of the Ca2+ release-activated Ca2+ channel.

42 tained elevation of intracellular calcium by Ca2+ release-activated Ca2+ channels is required for lym

43 s triggers Ca2+ entry through store-operated Ca2+ release-activated Ca2+ channels, promoting nuclear

44 that Ca2+ entry through store-operated CRAC (Ca2+ release-activated Ca2+) channels activates the extr

45 tassium currents (I IRK and I DRK), calcium (Ca2+) release-activated Ca2+ currents (I CRAC) and Ca2+-

46 the ER Ca2+ sensor and a prototypic SOC, the Ca2+-release-activated Ca2+ (CRAC) channel.

47 Rya-r44F, the ER Ca2+ sensor dSTIM, and the Ca2+-release-activated Ca2+ channel dOrai in the same pa

48 This local Ca2+ release activates nuclear CaMKII, which triggers HD

49 cyclic ADP ribose, NAADP-dependent lysosomal Ca2+ release, activation of the CaSR, or displacement of

50 though [Ca2+]SR exerts major influence on SR Ca2+ release, alternations in [Ca2+](SR) are not require

51 The Ca2+-induced Ca2+ release amplification factor or gain (SR Ca2+ relea

52 Although ryanodine receptor-mediated Ca2+ release amplifies the IP3R-induced trigger for the

53 thways (inositol-1,4,5-triphosphate-mediated Ca2+ release and activation of protein kinase C) were no

54 2-null mice are viable and display normal SR Ca2+ release and contractile function under basal condit

55 +-binding protein, is an enhancer of cardiac Ca2+ release and contractility and a potential therapeut

56 g in cardiac myocytes leading to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).

57 xhibited a significant decrease in lysosomal Ca2+ release and externalization of PS in response to ap

58 Thus, intracellular Ca2+ release and increases in cell survival after BCR cr

59 d disruption of the triad junctions impaired Ca2+ release and likely contributed to the mild permanen

60 time points during ISO application.While SR Ca2+ release and load reached a maximum level after 3 mi

61 were generated by the nonlinear dynamics of Ca2+ release and refilling in the SR.

62 diated enhancement of sarcoplasmic reticulum Ca2+ release and that PLCepsilon significantly enhances

63 icating that vWF/p.V1316M acts downstream of Ca2+ release and upstream of Rap1.

64 KI mice resulted primarily from enhanced RyR-Ca2+ release and were associated with increased RyR expr

65 significantly higher rate of spontaneous SR Ca2+ releases and triggered beats.

66 leak, resulting in premature spontaneous SR Ca2+ releases and triggered beats.

67 chondria to sequester Ca2+ in response to ER Ca2+ release, and increased mitochondrial ROS production

68 racellular Ca2+ rise, sarcoplasmic reticulum Ca2+ release, and intracellular Ca2+ decay rate.

69 in increased [Ca2+]SR and further enhance SR Ca2+ release at the next beat.

70 ve INa does not play a role in synchronizing Ca2+ release at the t-tubules; the amplitude of the Ca2+

71 se termination, and that abnormal fractional Ca2+ release attributable to aberrant termination of Ca2

72 tivity and ryanodine receptor (RyR)-mediated Ca2+ release, but underlying molecular mechanisms are po

73 sphorylation" of RyR2-S2808, which increases Ca2+ release by augmenting the sensitivity of the RyR2 c

74 how this to be the result of light-dependent Ca2+ release by bright background light, which can be ab

75 ese results suggest that CASQ2 stabilizes SR Ca2+ release by inhibiting the RyR2 channel through inte

76 reticulum, which suggests that intracellular Ca2+ release by InsP3R2 in clear cells of the sweat glan

77 bited reduced Ca2+ uptake and reduced stored Ca2+ release by UTP (400 microM) that activates a differ

78 C inhibitors, by inhibitors of intracellular Ca2+ release, by Pyk2-targeted siRNA, and by the Ras inh

79 racellular Ca2+ signaling, including quantal Ca2+ release, by tuning ligand sensitivities of InsP3R c

80 data indicate that loss of InsP3R2-mediated Ca2+ release causes isolated anhidrosis in humans and su

81 tic Ca2+ waves and DADs driven by stochastic Ca2+ release channel (RyR) gating and is used to study m

82 ositol 1,4,5-trisphosphate receptor (InsP3R) Ca2+ release channel and exert profound stimulatory effe

83 ine receptor has been mainly regarded as the Ca2+ release channel from sarcoplasmic reticulum control

84 Loss of JPH2 had profound effects on Ca2+ release channel inactivation, suggesting a novel fu

85 e activity of this lysosomal NAADP-sensitive Ca2+ release channel increased when the pH in cis soluti

86 native membrane-bound sarcoplasmic reticulum Ca2+ release channel is described.

87 ovide direct evidence that a NAADP-sensitive Ca2+ release channel is present in the lysosome of nativ

88 Ca2+ release that is intrinsic to the InsP3R Ca2+ release channel itself.

89 ing the ryanodine receptor 2, cardiac (RyR2)/Ca2+ release channel macromolecular complexes and the sa

90 The type 2 ryanodine receptor (RyR2) is a Ca2+ release channel on the endoplasmic reticulum (ER) o

91 uring exercise in mice and humans, the major Ca2+ release channel required for excitation-contraction

92 The Ca2+ release channel ryanodine receptor 2 (RyR2) is requ

93 nd characterized a lysosomal NAADP-sensitive Ca2+ release channel using purified lysosomes from rat l

94 membrane protein, the sarcoplasmic reticulum Ca2+ release channel with a molecular mass of 2.2 millio

95 ne receptor (RyR1), a sarcoplasmic reticulum Ca2+ release channel, in the mdx mouse model of muscular

96 ally relevant activator of the intracellular Ca2+ release channel, the ryanodine receptor isoform 1 (

97 elease evoked by activators of intracellular Ca2+ release channel/ryanodine receptor (10 mM caffeine,

98 has been linked to mutations in the cardiac Ca2+ release channel/ryanodine receptor (RyR2) located o

99 nodine receptor (RyR2) is the major calcium (Ca2+) release channel on the sarcoplasmic reticulum (SR)

100 ) and activation of its receptor (InsP3R), a Ca2+-release channel in the endoplasmic reticulum, is a

101 s of the type 2 ryanodine receptor (RyR2), a Ca2+-release channel present on the endoplasmic reticulu

102 leak in RyR2 channels with a novel class of Ca2+-release channel stabilizers called Rycals and (b) i

103 R membrane or by directly interacting with a Ca2+-release channel.

104 rs of intracellular ryanodine receptor (RyR) Ca2+ -release channels in mouse brain neurons, most prom

105 ctivates a different family of intracellular Ca2+ release channels (inositol 1,4,5-trisphosphate rece

106 m the concerted opening of a small number of Ca2+ release channels (ryanodine receptors, RyRs) organi

107 It was found that NAADP activates lysosomal Ca2+ release channels at concentrations of 1 nM to 1 mic

108 hanism is likely the direct regulation of SR Ca2+ release channels by Casq2 rather than altered lumin

109 late, continuing to progress even after the Ca2+ release channels have closed.

110 al role for JPH2 in regulating intracellular Ca2+ release channels in cardiac myocytes.

111 There are two forms of Ca2+ release channels on cardiac SR: type 2 ryanodine re

112 malemmal voltage-activated Ca2+ channels and Ca2+ release channels on sarcoplasmic reticulum within j

113 Either activators or blockers of Ca2+ release channels on the sarcoplasmic reticulum (SR)

114 e, the identity of lysosomal NAADP-sensitive Ca2+ release channels was also investigated.

115 Ryanodine receptors (RyRs)/Ca2+ release channels, on the endoplasmic and sarcoplasm

116 with TRP-ML1, which is different from ER/SR Ca2+ release channels.

117 ect on the activity of these NAADP-activated Ca2+ release channels.

118 ositol 1,4,5-trisphosphate receptor (IP(3)R)/Ca2+ release channels.

119 ably due to a change in the gating of the SR Ca2+-release channels and/or in their single channel flu

120 o generate IP3-mediated release of Ca2+ from Ca2+-release channels in the nucleus.

121 ted the hypothesis that altered Ca2+-induced Ca2+ release (CICR) from ryanodine receptors, which can

122 eceptor (betaAR) stimulation of Ca2+-induced Ca2+ release (CICR) in cardiac myocytes.

123 The contribution of Ca2+-induced Ca2+ release (CICR) to trigger muscle contraction is con

124 Rapid Ca2+ release correlated with colocalization of highly ph

125 Conversely, BCR-mediated intracellular Ca2+ release could be inhibited in CLL cells with low le

126 t remains unknown whether Casq2 regulates SR Ca2+ release directly or indirectly by buffering SR lumi

127 table to a failure of subcellular propagated Ca2+ release due to an increased cytosolic buffering str

128 In this study, Ca2+ release due to spontaneous Ca2+ waves was measured

129 ach to study the restitution of Ca2+-induced Ca2+ release during simulated two-pulse voltage-clamp pr

130 However, the extent of SR Ca2+ release during the small beats was smaller than exp

131 hey may support the process of intracellular Ca2+ release, either indirectly by manipulating ionic fl

132 role for spontaneous sarcoplasmic reticulum Ca2+ -release events in long-standing persistent AF, but

133 nce and mechanisms of sarcoplasmic reticulum Ca2+ -release events in paroxysmal AF (pAF) are unknown.

134 ticulum Ca2+ leak and sarcoplasmic reticulum Ca2+ -release events, causing delayed after-depolarizati

135 local diastolic sarcoplasmic reticulum (SR) Ca2+ release events (Ca2+ sparks) and RyR channel openin

136 yed Ca2+ transients and frequent spontaneous Ca2+ release events and at the whole heart level, increa

137 This allows hierarchical recruitment of Ca2+ release events as the InsP3 concentration increases

138 ntaneously giving rise to spatially-confined Ca2+ release events known as "sparks." RyR2s are organiz

139 tigate the mechanistic basis for spontaneous Ca2+ release events that lead to delayed afterdepolariza

140 n duration, and more frequent propagating SR Ca2+ release events were observed.

141 wn myotubes had significantly reduced stored Ca2+ release evoked by activators of intracellular Ca2+

142 Na inactivation produced a decline in the SR Ca2+ release flux (measured as the maximum rate of rise

143 cells of heterozygous YS mice we determined Ca2+ release flux activated by clamp depolarization, per

144 ms of Na+ channels, produced a decline in SR Ca2+ release flux of 35 +/- 3% (n = 6, P < 0.001) and tr

145 f cells exhibit synchronized, high amplitude Ca2+ release flux.

146 rtant insight into the role of IP3R-mediated Ca2+ release for pacemaker activity in differentiating c

147 tracaine (50 microM) reduced the spontaneous Ca2+ release frequency while increasing the Ca2+ wave am

148 version to total Ca2+ release suggested that Ca2+ release from a Ca2+ wave was not significantly diff

149 olipase C-gamma1 (PLC-gamma1) activation and Ca2+ release from inositol 1,4,5-trisphosphate receptor

150 the initial burst of secretion is driven by Ca2+ release from internal stores, but sustained exocyto

151 feine or thapsigargin, agents that stimulate Ca2+ release from internal stores.

152 try through AMPA receptors with a subsequent Ca2+ release from internal stores.

153 event for initiation of HPV, with consequent Ca2+ release from intracellular ryanodine-sensitive stor

154 have identified specific channels mediating Ca2+ release from intracellular stores and influx across

155 nce plate reader allows rapid measurement of Ca2+ release from intracellular stores mediated by IP3R.

156 isms behind quantal Ca2+ release, the graded Ca2+ release from intracellular stores through inositol

157 sitol 4,5-bisphosphate (PIP2) hydrolysis and Ca2+ release from intracellular stores via the phospholi

158 Ca2+ plateaus are not mediated by Ca2+ release from intracellular stores, but rather by an

159 se kinase-dependent pathway) that stimulates Ca2+ release from intracellular stores.

160 its effect through Ca2+ influx, rather than Ca2+ release from intracellular stores.

161 ase-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores.

162 n the absence of extracellular Ca2+ elicited Ca2+ release from intraterminal stores, a ryanodine-sens

163 These data indicate that although Ca2+ release from other intracellular organelles to the

164 ATP augmented InsP3-induced Ca2+ release from permeabilized cells expressing wild ty

165 Ca2+-induced Ca2+ release from presynaptic endoplasmic reticulum (ER)

166 a2+ sparks, which are the elemental units of Ca2+ release from sarcoplasmic reticulum, are silent und

167 ing both mitochondrial Ca2+ permeability and Ca2+ release from sarcoplasmic reticulum.

168 First, transient, PLC-dependent Ca2+ release from stores with precisely reproducible tim

169 CaM more than twofold by slowing the rate of Ca2+ release from the complex.

170 The antiapoptotic protein Bcl-2 inhibits Ca2+ release from the endoplasmic reticulum (ER).

171 and -deficient cells revealed that enhanced Ca2+ release from the endoplasmic reticulum as a result

172 Receptor-evoked Ca2+ signalling involves Ca2+ release from the endoplasmic reticulum, followed by

173 ng phospholipase C and subsequently inducing Ca2+ release from the endoplasmic reticulum, which plays

174 pore forming region of InsP3R2 and abrogates Ca2+ release from the endoplasmic reticulum, which sugge

175 Ca2+ channels and followed by Ca2+ -induced Ca2+ release from the endoplasmic reticulum.

176 the results obtained support the notion that Ca2+ release from the ER has little or no access to the

177 To assess the contribution of Ca2+ release from the ER in mediating the effects of ace

178 ATP-mediated IP3 production, the subsequent Ca2+ release from the ER through IP3R channels and ATP r

179 Ca2+ release from the ER was induced in isolated rat isl

180 on as a homeostatic response by Ca2+-induced Ca2+ release from the ER.

181 pacemaking, particularly in association with Ca2+ release from the sarcoplasmic reticulum (SR) that o

182 ocytes generate all-or-none APs, which evoke Ca2+ release from the sarcoplasmic reticulum (SR), altho

183 Diastolic Ca2+ release from the sarcoplasmic reticulum via "leaky"

184 cyte Ca2+ handling, particularly spontaneous Ca2+ release from the sarcoplasmic reticulum.

185 In mouse AM, AT structures triggered Ca2+ release from the SR approximately 2 times faster at

186 , another factor, possibly refractoriness of Ca2+ release from the SR contributes.

187 osed that the resulting supranormal calcium (Ca2+) release from the PC endoplasmic reticulum plays a

188 Calcium (Ca2+) released from the sarcoplasmic reticulum (SR) is c

189 Ca2+ release has a transient fast phase, whose rate is p

190 During exercise, defects in calcium (Ca2+) release have been proposed to impair muscle functi

191 The ATP sensitivity of InsP3-induced Ca2+ release, however, was not altered by the G1690A mut

192 a2+ release amplification factor or gain (SR Ca2+ release/I(Ca)) is usually assessed by the V(m) depe

193 , CSQ1 is not essential for effective stored Ca2+ release in C2C12 myotubes despite our in vitro stud

194 tely represent local control of Ca2+-induced Ca2+ release in cardiac myocytes can reproduce high-gain

195 ch to modeling local control of Ca2+-induced Ca2+ release in cardiac myocytes, where we derived coupl

196 ll immunophilin that stabilizes RyR-mediated Ca2+ release in cardiomyocytes, declines in hippocampus

197 To determine the basis of the reduced stored Ca2+ release in CSQ2 knockdown myotubes, we performed im

198 Overall, IP3R-mediated Ca2+ release in ESdCs is translated into a depolarizatio

199 ntal role in defining the characteristics of Ca2+ release in individual cell types.

200 ER stress induced by ER Ca2+ release in particular revealed fundamental differen

201 3R channel activity in vitro, IP3-induced ER Ca2+ release in permeabilized cells, and cell-permeable

202 smic reticulum (SR) that are responsible for Ca2+ release in rat ventricular myocytes.

203 pressed activation of sarcoplasmic reticulum Ca2+ release in S100A1-/- muscle fibers.

204 S100A1 modulation of sarcoplasmic reticulum Ca2+ release in striated muscle has not been fully eluci

205 tical role for junctophilin in intracellular Ca2+ release in the heart.

206 release, we measured I(Ca) and junctional SR Ca2+ release in voltage-clamped rat ventricular myocytes

207 Time-dependent refractoriness of calcium (Ca2+) release in cardiac myocytes is an important factor

208 principle channel for intracellular calcium (Ca2+) release in many cell types, including central neur

209 es have been proposed to account for quantal Ca2+ release, including the presence of heterogeneous ch

210 ted that FGF13 also regulated Ca(2+)-induced Ca2+ release, indicated by a smaller Ca2+ transient afte

211 mitochondrial Ca2+ uptake in response to ER Ca2+ release induced by thapsigargin or ATP.

212 is study challenge the current paradigm that Ca2+ release instability underlies AF.

213 t cell types, are required for intracellular Ca2+ release involved in diverse cellular functions, inc

214 ease attributable to aberrant termination of Ca2+ release is a common defect in RyR2-associated cardi

215 In cardiac muscle, intracellular Ca2+ release is controlled by a number of proteins inclu

216 In cardiomyocytes, RyR2-dependent Ca2+ release is critical for excitation-contraction coup

217 was similar, suggesting that the trigger for Ca2+ release is not altered by blocking TTX-sensitive IN

218 IP3R1-mediated Ca2+ release is regulated during oocyte maturation such

219 e plasma membrane (50%) whereas Ca2+-induced Ca2+ release is the major contributor to Ca2+ transients

220 bnormal activation of sarcoplasmic reticulum Ca2+ release is the primary cause of RyR2-associated car

221 total SR Ca2+ content in HF, and reduced SR Ca2+ release, is attributable to reduced [Ca2+]SR, not t

222 Local, rhythmic, subsarcolemmal Ca2+ releases (LCRs) from the sarcoplasmic reticulum (SR

223 rade regulation of the TT membrane on the SR Ca2+ release machinery.

224 ux via L-type Ca2+ channels and Ca2+-induced Ca2+ release mediated by clusters of ryanodine receptors

225 sient increases in [Ca2+]i via intracellular Ca2+ release mediated by the phospholipase C and inosito

226 ndogenous CIF production may be triggered by Ca2+ release (net loss) as well as by simple buffering o

227 ve stores are implicated in the Ca2+-induced Ca2+ release, NO can be expected to potentiate GABA rele

228 wed that activation of the K+ conductance by Ca2+ release occurred in small dendrites and subresoluti

229 However, once such a weak SR Ca2+ release occurs, it can result in increased [Ca2+]SR

230 e 2 calsequestrins (CSQ1 and CSQ2) in stored Ca2+ release of C2C12 skeletal muscle myotubes.

231 currents (ICa), charge movements (Q) and SR Ca2+ release of muscle fibres isolated from adult mice.

232 GTA in NCX KO mice reveals the dependence of Ca2+ release on NCX.

233 be elicited by stimulation of intracellular Ca2+ release or activation of protein kinase C.

234 athetic regulation of sarcoplasmic reticulum Ca2+ release or cardiac contractility.

235 We determined that less Ca2+ release per [Ca2+]i transient, increased Ca2+ buffe

236 k provides novel perspectives on the cardiac Ca2+ release process and a general method for inferring

237 tic events from a limited set of spontaneous Ca2+ release profiles is presented.

238 In all forms of alternans, the SR Ca2+ release rate was higher during large depletions tha

239 sting that control of sarcoplasmic reticulum Ca2+ release, rather than Ca2+ influx through L-type Ca2

240 l insight into beta-adrenergic regulation of Ca2+ release refractoriness in mouse myocytes.

241 hanism mediating NAADP-induced intracellular Ca2+ release remains unclear.

242 ellular stores and were able to increase the Ca2+-released response to a subthreshold dose of inosito

243 In conclusion, spontaneous Ca2+ release results in substantial but not complete loc

244 Ryanodine (10 microM), a ryanodine-sensitive Ca2+ release (RyR) channel blocker; iberiotoxin (100 nM)

245 investigation of the functions of NAADP as a Ca2+ -releasing second messenger.

246 This Ca2+ release silencing was attributable to a failure of

247 ANO1 is particularly tightly coupled to the Ca2+ release sites of the intracellular Ca2+ stores.

248 nal proteins that are located in or near the Ca2+ release sites.

249 h a three-dimensional array of functional SR Ca2+ release sites; however, in intact cells under resti

250 steepness of the sarcoplasmic reticulum (SR) Ca2+ release slope.

251 evation to trigger TRPML1-mediated lysosomal Ca2+ release specifically at the site of uptake, rapidly

252 Conversion to total Ca2+ release suggested that Ca2+ release from a Ca2+ wav

253 SR Ca2+ storage and altered caffeine-induced Ca2+ release, suggesting an orthograde regulation of the

254 For both control and HF myocytes, SR Ca2+ release terminated when [Ca2+]SR dropped to 0.3 to

255 reduced the luminal Ca2+ threshold at which Ca2+ release terminates and increased the fractional Ca2

256 Furthermore, measurements suggest that Ca2+ release terminates when luminal [Ca2+] reaches appr

257 lasia type 2, also reduced the threshold for Ca2+ release termination and increased fractional releas

258 te action (i.e., increased the threshold for Ca2+ release termination and reduced fractional release)

259 egion of RyR2 is an important determinant of Ca2+ release termination, and that abnormal fractional C

260 tion-contraction coupling produces high-gain Ca2+ release that is graded with changes in membrane pot

261 ation-contraction coupling produce high-gain Ca2+ release that is graded with changes in membrane pot

262 in cardiac myocytes can reproduce high-gain Ca2+ release that is graded with changes in membrane pot

263 R channels, providing a mechanism for graded Ca2+ release that is intrinsic to the InsP3R Ca2+ releas

264 rify the molecular mechanisms behind quantal Ca2+ release, the graded Ca2+ release from intracellular

265 Ca2+ release through all InsP3R family members is also m

266 inergic polymorphic VT is caused by enhanced Ca2+ release through defective ryanodine receptor (RyR2)

267 the phosphonothioate ccPA analogue inhibited Ca2+ release through LPA1/LPA3 activation and was an LPA

268 Intracellular Ca2+ release through ryanodine receptor (RyR) and inosit

269 dPt exhibited increased responsiveness of SR Ca2+ release to activation by ICa as manifested by flatt

270 pecific mechanism for coupling intracellular Ca2+ release to phosphorylation-dependent regulation of

271 coupling depends upon sarcoplasmic reticular Ca2+ release triggered by Ca2+ influx through L-type Ca2

272 plasmic reticulum (SR) [Ca2+] conditioned on Ca2+ release unit (CaRU) state.

273 Modeling Ca2+ release unit activity using this probability densit

274 arcoplasmic reticulum [Ca2+] conditioned on "Ca2+ release unit" state.

275 ed for a physiologically realistic number of Ca2+ release units and benchmarked for computational eff

276 f ryanodine receptors (RyR2) into functional Ca2+ release units is central to current models for card

277 ional SR [Ca2+] across a large population of Ca2+ release units is distinct on alternating cycles.

278 ch act as the major mediators of contractile Ca2+ release, upon a physiologically-realistic cellular

279 ar Ca2+signals are amplified by Ca2+-induced Ca2+ release via both ryanodine and IP3 receptors, which

280 3 production, elicits local nuclear envelope Ca2+ release via InsP3R.

281 igher potency of guanophostin 5 in assays of Ca2+ release via recombinant Ins(1,4,5)P3R are in agreem

282 sitive process designated as voltage-induced Ca2+ release (VICaR).

283 -Gly-Asp (RGD) mimetic, impaired HSV-induced Ca2+ release, viral entry, plaque formation, and cell-to

284 howed that for a given [Ca]SR, fractional SR Ca2+ release was actually higher in HF.

285 e number of sparks was restored in KO cells, Ca2+ release was asynchronous.

286 Thapsigargin-stimulated intracellular Ca2+ release was decreased in DD cells.

287 Ca2+ release was dramatically potentiated following acti

288 An intrastore surge upon induction of Ca2+ release was first reported in subcellular store fra

289 Ca2+ release was induced pharmacologically to activate S

290 h a timescale comparable to that for quantal Ca2+ release was observed under any steady ligand condit

291 and NP(o) separately influence Ca2+-induced Ca2+ release, we measured I(Ca) and junctional SR Ca2+ r

292 tion of the receptor and the potentiation of Ca2+ release were absent in cells expressing the G1690A

293 These alterations in SR Ca2+ release were accompanied by a significant decrease

294 The kinetics of Ca2+ release were biphasic, demonstrating a rapid elevat

295 Local Ca2+ signals during spontaneous Ca2+ release were compared with those induced by rapid c

296 ints of the voltage dependence of gCa, Q and Ca2+ release were not different from those in control fi

297 ion of transgenic proteins, while ICa, Q and Ca2+ release were studied electrophysiologically and opt

298 bits alternating sarcoplasmic reticulum (SR) Ca2+ release when periodically stimulated by depolarizin

299 g in cardiac myocytes occurs by Ca2+-induced Ca2+ release, where L-type Ca2+ current evokes a larger

300 (m) = 0 mV) may still effectively trigger SR Ca2+ release, whereas at positive V(m) (and smaller i(Ca