ライフサイエンスコーパス: CICR

1 CICR could not be triggered in the basal region, despite

2 CICR in response to forskolin was blocked by transient t

3 CICR is known to be coupled to Ca2+ entry in skeletal mu

4 CICR is the major process responsible for global Ca2+ tr

5 CICR required influx of Ca2+ through L-type voltage-depe

6 CICR triggered by flash photolysis of Nitr-5 appeared to

7 CICR triggered by photolysis of Nitr-5 appeared to be mo

8 CICR was evoked by the glucagon-like-peptide-1 (GLP-1) r

9 CICR was triggered by the GLP-1 receptor agonist exendin

10 CICR, in theory, is a high-gain, self-regenerating proce

11 Second, we incorporate the RyR model into a CICR model that has both a diadic space and the junction

12 local uncaging of Ca2+ was able to trigger a CICR wave, which propagated toward the base.

13 n of Ca2+ stores with thapsigargin abolishes CICR, while inhibitors of Ca2+ release channels (ryanodi

14 ent increase of [Ca(2+)](i) that accompanies CICR is shown to be coupled to exocytosis.

15 The increase of [Ca(2+)](i) that accompanies CICR stimulates the asynchronous release of a small numb

16 effects of cytosolic Ca2+, thereby allowing CICR to be generated by the uncaging of Ca2+ (UV flash p

17 This mechanism allows CICR-triggered synaptic release to be sustained indefini

18 udy provides the first evidence that altered CICR plays a role in driving the early and simultaneous

19 parameters, the SK2 channels activation and CICR rate.

20 s by successive cycles of Ca2+ diffusion and CICR.

21 utions of messenger-induced Ca2+ release and CICR.

22 es studied here, internal calcium stores and CICR do not contribute to short-term presynaptic plastic

23 ardiomyocyte t-tubule and cell structure and CICR over time and following mechanical overload.

24 e channels (ryanodine and heparin) attenuate CICR in an additive manner.

25 The augmented CICR observed after arrest was mediated by the activatio

26 t both ryanodine and intracellular Cs+ block CICR in inner hair cells.

27 th the cAMP antagonist 8-Br-Rp-cAMPS blocked CICR in response to exendin-4, whereas the PKA inhibitor

28 Blocking CICR inhibits >50% of release from rods in darkness.

29 Blocking CICR resulted in mixed action potential waveforms with b

30 Blocking CICR with 10 microM ryanodine reduced DAP amplitude by a

31 Furthermore, selectively blocking CICR with ryanodine slowed the Ca2+ rise during synaptic

32 in part through BK channels, is activated by CICR at membrane voltages approaching the threshold for

33 n potential propagation and amplification by CICR.

34 e rat fibres there is little contribution by CICR to Ca2+ release triggered by depolarization, and a

35 nj-SR, activated in a centripetal fashion by CICR via I(Ca) and Ca(2+) release from j-SR, respectivel

36 on in IP3 binding and channel recruitment by CICR further determine puff amplitudes.

37 n of Ca2+ from the majority of the stores by CICR.

38 ce cisterna of the OHC, perhaps triggered by CICR from the synaptic cisterna; the two time scales of

39 plicating Epac for the first time in cardiac CICR.

40 Finally, although caffeine causes CICR in Purkinje cell bodies and dendrites, it does not

41 Therefore the responses qualify as 'classic' CICR.

42 In contrast, CICR recovery was slowed by eliminating the Na(+)/Ca(2+)

43 al Ca2+ regulatory mechanisms in controlling CICR, we assessed the impact of intra-SR Ca2+ buffering

44 ng of the activation threshold for cytosolic CICR.

45 The present study demonstrates CICR in the non-excitable parotid acinar cells, which re

46 nificantly inhibited isoproterenol-dependent CICR.

47 n, ryanodine or 200 microM Cd(2+) to disrupt CICR decreased the latency to AP generation during 400 m

48 Fractional utilization of Ca2+ stores during CICR increased with the degree of Ca2+ loading.

49 When [Ca(2+)](B) is slightly elevated, CICR targets a much larger pool of secretory granules th

50 ell bodies and dendrites, it does not elicit CICR in parallel fiber inputs to these cells.

51 centrations of ryanodine to block or enhance CICR to determine whether calcium release from intracell

52 ivity of the IP(3)R to Ca(2+), i.e. enhanced CICR, and suggest that glutathionylation may represent a

53 levating agents such as exendin-4 facilitate CICR in beta-cells by activating both protein kinase A a

54 srupts the action of exendin-4 to facilitate CICR in the beta-cells of these mice.

55 8-pCPT-2'-O-Me-cAMP-AM failed to facilitate CICR in WT beta-cells transduced with a GTPase activatin

56 This action of exendin-4 to facilitate CICR was reproduced by cAMP analogues that activate prot

57 tion of 8-pCPT-2'-O-Me-cAMP-AM to facilitate CICR, whereas a K2150E PLC- with a mutated Ras associati

58 A relative refractory period followed CICR.

59 om hippocampal slices, we found evidence for CICR during action potential-evoked Ca2+ transients.

60 eptor inner segments, and suggest a role for CICR in the regulation of synaptic transmission.

61 IHCs can generate CICR, but to date its physiological role has remained un

62 lysis-catalysed uncaging of Ca(2+) generated CICR in only 9% of the beta-cells tested, whereas CICR w

63 ly encoded calcium sensor, GCaMP6f, to image CICR in vivo.

64 This decrease in CICR activity was partially recovered by pretreatment wi

65 from calcineurin), resulted in a decrease in CICR.

66 ave shown that betaAR-dependent increases in CICR consist of two independent components mediated by P

67 oth betaAR- and Epac-stimulated increases in CICR in PLCepsilon+/+ myocytes but had no effect in PLCe

68 VGCC current and the sAHP and also increased CICR.

69 els generate 60% of action potential-induced CICR, only Ca2+ influx through N type Ca2+ channels can

70 ICR by apical uncaging, and uncaging-induced CICR could activate long-lasting Ca2+ oscillations.

71 f the polyamine/K(ATP) channel/Ca(2+) influx/CICR pathway not only boosted the vulnerability of retin

72 g the polyamine/K(ATP) channel/Ca(2+) influx/CICR pathway.

73 Peripheral elevation of [Ca(2+) ]i initiates CICR from nj-SR and sustains propagation of CICR to the

74 These results provide critical insights into CICR dynamics in heart, under normal and pathological co

75 , and RyR1s alone are able to support inward CICR propagation in most cells at an average speed of ap

76 loads produce larger currents (ie, a larger CICR trigger signal).

77 To maintain CICR as rods remain depolarized in darkness, we hypothes

78 ntly inhibited both betaAR and Epac-mediated CICR enhancement.

79 r, KN93, inhibited betaAR- and Epac-mediated CICR in PLCepsilon+/+ but not PLCepsilon-/- myocytes.

80 (CICR) and that RyR3 amplifies RyR1-mediated CICR in neonatal skeletal muscle.

81 ctly triggered SR Ca2+ release nor modulated CICR in intact myocytes.

82 rd current and [Ca2+](i) suggested that most CICR triggered by Ca2+ influx occurred away from the pla

83 under near physiological conditions, neither CICR nor Na(+)-Ca2+ exchange play a substantial role in

84 no-cADPR, was ineffective in altering normal CICR in myocytes.

85 findings provide evidence for activation of CICR by Ca2+ influx in non-excitable cells, demonstrate

86 thoxydiphenyl borate prevented activation of CICR observed on addition of external Ca2+.

87 ed responses that had the characteristics of CICR.

88 We discuss the contribution of CICR to the measured [Ca2+]i transient, the implications

89 , and those that do include local control of CICR are able to reconstruct properties of EC coupling,

90 riving simplified models of local control of CICR, consisting of low-dimensional systems of coupled o

91 providing for both the voltage-dependence of CICR and the higher frequency of spark occurrence in the

92 es of Epac2 and PLC- are key determinants of CICR in this cell type.

93 The overall facilitatory effect of CICR on glutamate release induced during trains of actio

94 The fundamental element of CICR in the heart is the calcium (Ca(2+)) spark, which a

95 a role in the beta-adrenergic enhancement of CICR by effectively contributing to the Ca(2+) trigger.

96 The inherent positive feedback of CICR is normally well-controlled.

97 urred within 5 s following the initiation of CICR.

98 contrary to the physiological involvement of CICR in mammalian excitation-contraction coupling.

99 Here we tested for the involvement of CICR in short-term presynaptic plasticity at six excitat

100 the results suggest that despite the lack of CICR, the SR removes Ca(2+) from the cytosol after its e

101 in terminating the positive feedback loop of CICR.

102 or deriving simplified mechanistic models of CICR to formulate an integrative model of the canine car

103 esult for the effects of other modulators of CICR are discussed.

104 tivity, the result supports participation of CICR in the physiological control of contraction in amph

105 he extent to which the regenerative phase of CICR can be supported by the partially depleted junction

106 We found potentiation of CICR in isolated cells from this extracorporeal membrane

107 m stores with thapsigargin and prevention of CICR with ryanodine have no effect on paired-pulse facil

108 CICR from nj-SR and sustains propagation of CICR to the cell centre.

109 ting [Ca(2+)](i), accelerated propagation of CICR, decreased extrusion of Ca(2+) and an increase in j

110 in C2C12 cells resulted in up-regulation of CICR.

111 V ) has emerged as an important regulator of CICR both in health and in disease.

112 results establish LMO4 as a key regulator of CICR in central neurons, providing a mechanism for LMO4

113 rse tubule system, the RyR3 reinforcement of CICR seems to ensure a robust, uniform, and synchronous

114 The start of CICR termination was strongly dependent on the extent of

115 strate a role for Epac in the stimulation of CICR, cardiac myocytes were treated with an Epac-selecti

116 -SR [Ca2+] is responsible for termination of CICR and for the subsequent restitution behavior of Ca2+

117 The termination of CICR by induction decay in the model principally arose f

118 The triggering of CICR from the apical region was inhibited by a pharmacol

119 A direct effect of 8-amino-cADPR on CICR cannot be excluded, but observations with caffeine

120 that Epac/PLC(epsilon)-dependent effects on CICR are independent of sarcoplasmic reticulum loading a

121 el of Ca(2+) indicated the effect of EGTA on CICR was due to buffering of released mitochondrial Ca(2

122 and it may thus exert a negative feedback on CICR in heart cells.

123 t prevented the inhibitory effect of NADH on CICR in isolated membranes and permeabilized cells, as w

124 in hypertonic solutions, thereby permitting CICR to operate even in such fully polarized skeletal mu

125 l signal transduction whereby GLP-1 promotes CICR by sensitizing intracellular Ca2+ release channels

126 ded to initiate regenerative and propagating CICR from nj-SR.

127 (2+) from the cell periphery and propagating CICR.

128 RyR3 in wild-type cells, unmitigated radial CICR propagates at 2,440 microm/s.

129 Here we show that regenerative CICR develops as an all-or-none event in cultured rat do

130 nge factor, Epac, and PLC(epsilon) regulates CICR in cardiac myocytes.

131 cid revealed that Ca2+ influx that regulates CICR is associated with a selective portion of the inter

132 ocess termed Ca(2+) -induced Ca(2+) release (CICR) - followed by re-sequestration of Ca(2+) into the

133 pling between Ca(2+)-induced Ca(2+) release (CICR) and quantal exocytosis in 5-hydroxytryptamine-load

134 both VICR and Ca(2+)-induced Ca(2+) release (CICR) and that RyR3 amplifies RyR1-mediated CICR in neon

135 triggered by Ca(2+)-induced Ca(2+) release (CICR) from intracellular stores.

136 ry activates Ca(2+) -induced Ca(2+) release (CICR) from j-SR ryanodine receptor (RyR) Ca(2+) release

137 CC) activity, Ca(2+)-induced Ca(2+) release (CICR) from ryanodine receptors (RyRs), and Ca(2+) transi

138 ike triggered Ca(2+)-induced Ca(2+) release (CICR) from the ER immediately beneath somatic, but not a

139 modulation of Ca(2+)-induced Ca(2+) release (CICR) from the sarcoplasmic reticulum (SR) by localized

140 m where local Ca(2+)-induced Ca(2+) release (CICR) from the sarcoplasmic reticulum (SR) via ryanodine

141 uggested that Ca(2+)-induced Ca(2+) release (CICR) from the SR did not contribute significantly to th

142 nhanced the caffeine-induced Ca(2+) release (CICR) in C2C12 cells.

143 timulation of Ca(2+)-induced Ca(2+) release (CICR) in cardiac myocytes.

144 ion coupling, Ca(2+)-induced Ca(2+) release (CICR) in particular, and transverse (t)-tubule structure

145 Calcium (Ca(2+))-induced Ca(2+) release (CICR) is widely accepted as the principal mechanism link

146 s disrupt the Ca(2+)-induced Ca(2+) release (CICR) process that mediates channel-channel coordination

147 duce a graded Ca(2+)-induced Ca(2+) release (CICR) response, CICR with high gain, and a system with r

148 l load and Ca(2) (+)-induced Ca(2+) release (CICR) simultaneously using the microcarbon fiber techniq

149 by activating Ca(2+)-induced Ca(2+) release (CICR) stores with 10 mM caffeine were not significantly

150 scriptions of Ca(2+)-induced Ca(2+) release (CICR) that account for these local mechanisms are lackin

151 ng successive Ca(2+)-induced Ca(2+) release (CICR) via Ca(2+) diffusion between adjacent elements.

152 ggesting that Ca(2+)-induced Ca(2+) release (CICR) via the IP(3)R is enhanced by glutathionylation.

153 mechanism of Ca(2+)-induced Ca(2+) release (CICR), and cAMP-elevating agents such as exendin-4 facil

154 a process of Ca(2+)-induced Ca(2+) release (CICR), and it generates an increase of [Ca(2+)](i) that

155 rticularly in Ca(2+)-induced Ca(2+) release (CICR), and its structural disruption is an early event i

156 oothly graded Ca(2+)-induced Ca(2+) release (CICR), which exhibits high gain.

157 Epac-mediated Ca(2+)-induced Ca(2+) release (CICR).

158 triggered by Ca(2+)-induced Ca(2+) release (CICR).

159 oordinated by Ca(2+)-induced Ca(2+) release (CICR).

160 a(2+) influx, Ca(2+)-induced Ca(2+)-release (CICR), and store-operated Ca(2+) influx.

161 of IP3 or by Ca(2+)-induced Ca(2+)-release (CICR).

162 parks by potentiating Ca-induced Ca release (CICR).

163 or cAMP-dependent Ca2+-induced Ca2+ release (CICR) from endoplasmic reticulum Ca2+ stores was assesse

164 Ca2+-induced Ca2+ release (CICR) from intracellular stores amplifies the Ca2+ signa

165 the properties of Ca2+-induced Ca2+ release (CICR) from isolated sites is used to explain this saltat

166 nwardly through Ca(2+)-induced Ca2+ release (CICR) from non-junctional SR (nj-SR).

167 esis that altered Ca2+-induced Ca2+ release (CICR) from ryanodine receptors, which can be triggered b

168 2 (RyR2)-mediated Ca2+-induced Ca2+ release (CICR) from SR membranes (IC50=120 micromol/L) and signif

169 ly termination of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) in cardiac mu

170 CX) in activating Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) in cardiac my

171 2+ sensitivity of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum.

172 Calcium (Ca2+)-induced Ca2+ release (CICR) in cardiac myocytes exhibits high gain and is grad

173 R) stimulation of Ca2+-induced Ca2+ release (CICR) in cardiac myocytes.

174 termination of Ca(2+)-induced Ca2+ release (CICR) in heart.

175 and to modulate Ca(2+)-induced Ca2+ release (CICR) in intact rat ventricular myocytes.

176 ding evidence for Ca2+-induced Ca2+ release (CICR) in rods and cones.

177 cts of modulating Ca2+-induced Ca2+ release (CICR) in single cardiac myocytes were investigated using

178 Ca2+-induced Ca2+ release (CICR) is a well characterized activity in skeletal and c

179 ide evidence that Ca2+-induced Ca2+ release (CICR) may contribute to the mechanism.

180 Ca2+-induced Ca2+ release (CICR) plays an important role in the generation of cytos

181 an intracellular Ca2+-induced Ca2+ release (CICR) pool.

182 hastic methods, Ca(2+)-induced Ca2+ release (CICR) shows both high gain and graded Ca2+ release that

183 lect a process of Ca2+-induced Ca2+ release (CICR) that requires activation of protein kinase A (PKA)

184 e contribution of Ca2+-induced Ca2+ release (CICR) to trigger muscle contraction is controversial.

185 myocytes, Ca2+ influx-induced Ca2+ release (CICR) utilized a greater fraction of caffeine-releasable

186 the threshold for Ca2+-induced Ca2+ release (CICR) was able to simulate each observed pattern by vary

187 Alternatively, Ca2+-induced Ca2+ release (CICR) was triggered by a rapid increase in [Ca2+] induce

188 IP3Rs display Ca2+-induced Ca2+ release (CICR), but are grouped in clusters so that regenerative

189 Ca) gives rise to Ca2+-induced Ca2+ release (CICR), the amplifying Ca2+ signaling mechanism that trig

190 GLP-1 facilitates Ca2+-induced Ca2+ release (CICR), whereby mobilization of Ca2+ stores is triggered

191 edback process of Ca2+-induced Ca2+ release (CICR).

192 in the process of Ca2+-induced Ca2+ release (CICR).

193 depression of calcium-induced Ca2+ release (CICR).

194 the properties of Ca2+-induced Ca2+-release (CICR) and the local control theory of excitation-contrac

195 dicative of calcium-induced calcium release (CICR) activity were induced in fully polarized, fluo-3-l

196 implicating calcium-induced calcium release (CICR) as the novel source of the Ca(i)(2+).

197 egenerative calcium-induced calcium release (CICR) during Ca(2+) spark evolution remain unclear.

198 an aberrant calcium-induced calcium release (CICR) effect within spines and dendrites.

199 oposed that calcium-induced calcium release (CICR) from a near-membrane postsynaptic store supplement

200 mplified by calcium-induced calcium release (CICR) from intracellular calcium stores.

201 ceptors and calcium-induced calcium release (CICR) from intracellular calcium stores.

202 (I(Ca)) of calcium-induced calcium release (CICR) from the junctional-SR (j-SR, in the subsarcolemma

203 4 regulates calcium-induced calcium release (CICR) in central neurons.

204 Calcium-induced calcium release (CICR) is a mechanism by which local elevations of intrac

205 Stable calcium-induced calcium release (CICR) is critical for maintaining normal cellular contra

206 or requires calcium-induced calcium release (CICR) is not yet known.

207 bably via a calcium-induced calcium release (CICR) mechanism.

208 ish whether calcium-induced calcium release (CICR) modulated action potential (AP) generation in mamm

209 stores and calcium-induced calcium release (CICR) provide an important source of calcium that drives

210 significant calcium-induced calcium release (CICR) since (i)[Ca2+]i scaled with the integrated I(Ca)

211 The gain of calcium-induced calcium release (CICR) was increased at all membrane potentials but espec

212 nhibitor of calcium-induced calcium release (CICR), dantrolene.

213 odulator of calcium-induced calcium release (CICR), had no effect on the spontaneous [Ca2+]i or force

214 ication via calcium-induced calcium release (CICR).

215 agonist of calcium-induced calcium release (CICR).

216 elease of Ca2+ via Ca2+-induced Ca2+ release(CICR).

217 agation (via calcium-induced Ca(2+) release, CICR) to the cell centre, resulting in contraction.

218 a2+ influx-gated (Ca2+-induced Ca2+ release, CICR) sarcoplasmic reticulum (SR) Ca2+ release were stud

219 e that CICR in non-excitable cells resembles CICR in cardiac myocytes with the exception that in card

220 (2+)-induced Ca(2+) release (CICR) response, CICR with high gain, and a system with reasonable stabil

221 the increased load, Ca(2+) spark (inter-RyR CICR events) frequency decreased and sparks terminated e

222 is no longer sufficient to sustain inter-RyR CICR.

223 RyR current amplitude that drives inter-RyR CICR.

224 To the left of the node, RyR/CICR and H(+)V-ATPase activity sustained elevated Ca(i)(

225 ted Ca(2+) influx followed by EGTA-sensitive CICR from the mitochondria.

226 vel of activity of the ER Ca2+ pump (SERCA), CICR and release-activated Ca2+ transport (RACT).

227 We conclude that RACT, SERCA, CICR and Ca2+-dependent PM Ca2+ influx are major mechani

228 ause the uncaging of Ca2+ fails to stimulate CICR in the absence of cAMP-elevating agents, it is conc

229 However, with subthreshold stimulation, CICR could still not be initiated in the basal region.

230 e-dependent gain, inconsistent with a strict CICR mechanism, suggesting the existence of additional r

231 disruptions in RyR signaling and subsequent CICR via NMDAR-mediated calcium influx alters synaptic f

232 raterminal ER Ca(2+) stores and thus sustain CICR-mediated synaptic release.

233 oplasmic reticulum (ER) to support sustained CICR-driven synaptic transmission?

234 mV are thought to represent VDCR rather than CICR.

235 It is concluded that CICR in INS-1 cells results from GLP-1 receptor-mediated

236 It is concluded that CICR is a highly effective stimulus for exocytosis in IN

237 kewise defective in LMO4 KO, confirming that CICR machinery is severely compromised in these neurons.

238 We established that CICR potentiation begins in vivo.

239 We found that CICR modulation of the afterhyperpolarization in CA3 neu

240 influx in triggering CICR, and indicate that CICR in non-excitable cells resembles CICR in cardiac my

241 These results indicate that CICR plays little role in SR Ca2+ release from the myome

242 Our data show that CICR forms an important component of the calcium signal

243 We show that CICR local control is governed by SR Ca(2+) load, largel

244 Confocal imaging experiments showed that CICR facilitated propagation of the Ca2+ signal from the

245 The CICR mechanism has been understood mainly based on bindi

246 The relationship predicted by the CICR hypothesis is bell-shaped with no contraction at EC

247 All results could be accounted for by the CICR hypothesis, and many results exclude the VDCR hypot

248 ces exhibited differential efficacies in the CICR assay such that exendin-4 was partly effective, 6-B

249 energic stimulation enhances the gain of the CICR cascade by increasing the fidelity of dihydropyridi

250 Characterization of the CICR mechanism by voltage clamp analysis also demonstrat

251 t UN leads to a functional uncoupling of the CICR process and identify disruption of the t-tubule-sar

252 Consistent with the importance of the CICR-dependent increase in capillary cell calcium, dantr

253 One possibility is that cADPR sensitizes the CICR mechanism to Ca2+, an action antagonized by 8-amino

254 We have directly tested the CICR sensitivity of different regions of intact pancreat

255 through N type Ca2+ channels can trigger the CICR-dependent AHPslow.

256 Furthermore, this CICR model produces a nonlinear relationship between fra

257 r cell efficiently couples synaptic input to CICR.

258 d intracellular variations in sensitivity to CICR predetermine the activation pattern of Ca2+ waves.

259 ave and primes RyRs from the luminal side to CICR.

260 the interaction of cAMP and Epac to trigger CICR explains, at least in part, the blood glucose-lower

261 s on catfish cone horizontal cells triggered CICR from ryanodine-sensitive stores and mimicked inhibi

262 ecognized role for Ca2+ influx in triggering CICR, and indicate that CICR in non-excitable cells rese

263 tion increased the probability of triggering CICR by apical uncaging, and uncaging-induced CICR could

264 The entry of Ca2+ during an AP triggers CICR from up to 20 or more subplasmalemmal store sites (

265 ia either L or N type Ca2+ channels triggers CICR.

266 suppresses long-lasting sparks by weakening CICR.

267 In contrast, when CICR is already strong enough to produce frequent firing

268 in only 9% of the beta-cells tested, whereas CICR was generated in 82% of the beta-cells pretreated w

269 While CICR provides for robust triggering of Ca2+ sparks, the

270 the strength of regenerative feedback within CICR.