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 disrupted in cardiac hypertrophy and heart failu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 parameters, the SK2 channels activation and CICR rate.

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

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

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

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

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

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

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

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

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

30 Blocking CICR resulted in mixed action potential waveforms with b

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

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

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

34 n potential propagation and amplification by CICR.

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

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

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

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

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

40 plicating Epac for the first time in cardiac CICR.

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

42 Therefore the responses qualify as 'classic' CICR.

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

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

45 ng of the activation threshold for cytosolic CICR.

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

47 nificantly inhibited isoproterenol-dependent CICR.

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

49 redistributed from the T-tubules to disrupt CICR.

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

51 l sarcoplasmic reticulum to ensure efficient CICR.

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

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

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

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

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

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

58 8-pCPT-2'-O-Me-cAMP-AM failed to facilitate CICR in WT beta-cells transduced with a GTPase activatin

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

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

61 A relative refractory period followed CICR.

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

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

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

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

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

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

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

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

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

71 VGCC current and the sAHP and also increased CICR.

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

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

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

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

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

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

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

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

80 can be used to measure the kinetics of local CICR recovery, alterations of which may be related to pr

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

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

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

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

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

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

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

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

89 cilitates dyad assembly and maintains normal CICR in cardiomyocytes.

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

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

92 ed responses that had the characteristics of CICR.

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

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

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

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

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

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

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

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

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

102 urred within 5 s following the initiation of CICR.

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

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

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

106 in terminating the positive feedback loop of CICR.

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

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

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

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

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

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

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

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

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

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

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

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

119 lecting both SR refilling and restoration of CICR and RyR Ca(2+) sensitivity.

120 and revealed a higher Ca(2+) sensitivity of CICR.

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

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

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

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

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

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

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

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

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

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

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

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

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

134 (2+) from the cell periphery and propagating CICR.

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

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

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

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

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

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

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

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

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

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

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

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

147 iac myocytes Ca(2+) -induced Ca(2+) release (CICR) from the sarcoplasmic reticulum (SR) through ryano

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 2 (RyR2)-mediated Ca2+-induced Ca2+ release (CICR) from SR membranes (IC50=120 micromol/L) and signif

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

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

179 2+ sensitivity of Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 4 regulates calcium-induced calcium release (CICR) in central neurons.

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

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

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

215 mooth ER, a calcium-induced calcium release (CICR) is triggered at the base of the spine by the faste

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

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

218 be due to a calcium induced calcium release (CICR) process that is initiated by outer cell membrane b

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

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

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

222 In calcium-induced calcium release (CICR), calcium ions flowing through activated CaV1 chann

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

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

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

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

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

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

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

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

231 (2+)-induced Ca(2+) release (CICR) response, CICR with high gain, and a system with reasonable stabil

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

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

234 RyR current amplitude that drives inter-RyR CICR.

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

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

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

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

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

240 e of cAMP or low-dose caffeine (to stimulate CICR) or cyclopiazonic acid (CPA; to slow SR refilling).

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

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

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

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

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

246 mV are thought to represent VDCR rather than CICR.

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

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

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

250 We established that CICR potentiation begins in vivo.

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

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

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

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

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

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

257 The CICR mechanism has been understood mainly based on bindi

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

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

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

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

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

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

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

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

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

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

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

269 r cell efficiently couples synaptic input to CICR.

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

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

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

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

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

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

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

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

278 suppresses long-lasting sparks by weakening CICR.

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

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

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

282 lusively in vertebrate skeletal muscle while CICR occurs in all other muscles (including all inverteb

283 the strength of regenerative feedback within CICR.