ライフサイエンスコーパス: excitation-contraction coupling

1 ion, and disarray of muscle triads (sites of excitation- contraction coupling).

2 ng that weakness was largely due to impaired excitation contraction coupling.

3 rafish shows that the NAM mutation decreases excitation-contraction coupling.

4 and supported beta-adrenergic regulation of excitation-contraction coupling.

5 a(2+)](mito) gradients quantitatively during excitation-contraction coupling.

6 discs, while NBC locally protects t-tubular excitation-contraction coupling.

7 voltage-sensing function in skeletal muscle excitation-contraction coupling.

8 asmic reticulum, an essential step in muscle excitation-contraction coupling.

9 ed contractile efficiency, restoring cardiac excitation-contraction coupling.

10 --the three prerequisites of skeletal muscle excitation-contraction coupling.

11 (2+) influx via L-type Ca(2+) current during excitation-contraction coupling.

12 l, CaV1.2, which plays a key role in cardiac excitation-contraction coupling.

13 gating, thereby amplifying Ca(2+) influx and excitation-contraction coupling.

14 ysiological involvement of CICR in mammalian excitation-contraction coupling.

15 tively, where they play an essential role in excitation-contraction coupling.

16 ffects likely to preserve functional myocyte excitation-contraction coupling.

17 it to the membrane and its suggested role in excitation-contraction coupling.

18 eletal muscle acts as the voltage sensor for excitation-contraction coupling.

19 nduced Ca release, and more ventricular-like excitation-contraction coupling.

20 fitting provides novel insights into cardiac excitation-contraction coupling.

21 , limiting spatial [Ca](SR) gradients during excitation-contraction coupling.

22 Pase responsible for Ca(2+) re-uptake during excitation-contraction coupling.

23 r local SR Ca release at low [Ca](SR) during excitation-contraction coupling.

24 n response to depolarization, referred to as excitation-contraction coupling.

25 omyocytes including electrical signaling and excitation-contraction coupling.

26 s and abnormal escape response, and impaired excitation-contraction coupling.

27 rived cardiomyocytes demonstrated functional excitation-contraction coupling.

28 lease from the sarcoplasmic reticulum during excitation-contraction coupling.

29 tionally efficient whole cell simulations of excitation-contraction coupling.

30 muscle responsible for calcium transport and excitation-contraction coupling.

31 calcium channels and play important role in excitation-contraction coupling.

32 bes but have little or no effect on skeletal excitation-contraction coupling.

33 sarcoplasmic reticulum Ca(2+) release during excitation-contraction coupling.

34 cium cycling is a vital component of cardiac excitation-contraction coupling.

35 channel openings are required for efficient excitation-contraction coupling.

36 he triad but not in regulating skeletal-type excitation-contraction coupling.

37 Ca(2+) release through RyRs controls muscle excitation-contraction coupling.

38 g that Cys-3635 is involved in voltage-gated excitation-contraction coupling.

39 acellular Ca2+ known as Ca2+ sparks regulate excitation-contraction coupling.

40 membranes in muscle cells ensuring efficient excitation-contraction coupling.

41 and propagation of the action potential and excitation-contraction coupling.

42 on of intracellular Ca2+ cycling and cardiac excitation-contraction coupling.

43 + exchanger may be an important regulator of excitation-contraction coupling.

44 lular [Ca(2+)] regulation and, consequently, excitation-contraction coupling.

45 parate (and insulated) from that involved in excitation-contraction coupling.

46 gulation of key proteins involved in cardiac excitation-contraction coupling.

47 cell core, ensuring synchronous and uniform excitation-contraction coupling.

48 ndrial function, glucose uptake, fatigue and excitation-contraction coupling.

49 nment or cell size, suggesting maturation of excitation-contraction coupling.

50 beta1a subunit in supporting skeletal muscle excitation-contraction coupling.

51 ular X-ROS signaling and its role in cardiac excitation-contraction coupling.

52 and is involved in the regulation of cardiac excitation-contraction coupling.

53 asmic calcium concentration ([Ca2+]i) during excitation-contraction coupling.

54 lar processes, such as energy metabolism and excitation-contraction coupling.

55 yanodine receptor type 2 plays a key role in excitation-contraction coupling.

56 ryanodine receptor (RyR1), are essential for excitation-contraction coupling.

57 faster kinetics than global [Ca(2+)]i during excitation-contraction coupling.

58 Ca(2+) flux in skeletal muscle that mediates excitation-contraction coupling.

59 rom the sarcoplasmic reticulum that mediates excitation-contraction coupling.

60 g normal cellular contraction during cardiac excitation-contraction coupling.

61 to fatigue, rhabdomyolysis and disruption of excitation-contraction coupling.

62 and muscle transverse (T) tubules facilitate excitation:contraction coupling.

63 In skeletal muscle excitation-contraction coupling, a voltage-gated calcium

64 from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including

65 ocytes, impaired contractility, and abnormal excitation-contraction coupling activities.

66 um Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias (3-4 Mar

67 is Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias Symposiu

68 4: Systems approach to understanding cardiac excitation-contraction coupling and arrhythmias: Na(+) c

69 4: Systems approach to understanding cardiac excitation-contraction coupling and arrhythmias: Na(+) c

70 effects of increased expression of miR-1 on excitation-contraction coupling and Ca(2+) cycling in ra

71 ntal evidence of transmural heterogeneity of excitation-contraction coupling and calcium handling in

72 rticle was to study functional remodeling of excitation-contraction coupling and calcium handling in

73 ociated with the heterogeneous remodeling of excitation-contraction coupling and calcium handling.

74 the functional impact of phosphorylation in excitation-contraction coupling and cardiac performance

75 of classes of protein targets important for excitation-contraction coupling and cell survival, inclu

76 cle Ca(2+) channel Ca(V)1.1, which initiates excitation-contraction coupling and conducts L-type Ca(2

77 c Ca(2+) signaling in skeletal muscle during excitation-contraction coupling and establishes that mal

78 key cardiac physiological roles, regulating excitation-contraction coupling and exerting an antioxid

79 suggest that the remodeled t-system impairs excitation-contraction coupling and functional recovery

80 further define the role of sorcin in cardiac excitation-contraction coupling and highlight its negati

81 Calcium cycling figures prominently in excitation-contraction coupling and in various signaling

82 d resting membrane potential, which modifies excitation-contraction coupling and increases proinflamm

83 ion through divergent mechanisms that impair excitation-contraction coupling and may be exemplary of

84 Despite TATS's crucial role in excitation-contraction coupling and morphological altera

85 We evaluated excitation-contraction coupling and nitroso-redox balanc

86 +) in normal cardiac function-in particular, excitation-contraction coupling and normal electric rhyt

87 RyRs play a major role in excitation-contraction coupling and other Ca(2+)-depende

88 messengers important for modulating cardiac excitation-contraction coupling and pathophysiology.

89 context of whole-cell electrophysiology, (3) excitation-contraction coupling and regulatory pathways,

90 on T4826I within the S4-S5 linker influences excitation-contraction coupling and resting myoplasmic C

91 we explore the effects of DP4 on orthograde excitation-contraction coupling and retrograde RyR1-DHPR

92 ation reserve of fly hearts, ensuring normal excitation-contraction coupling and rhythmical contracti

93 Ca(2+) is central to cardiac excitation-contraction coupling and stimulates mitochond

94 integral role in cellular processes such as excitation-contraction coupling and store-operated calci

95 els critical for skeletal and cardiac muscle excitation-contraction coupling and synaptic transmissio

96 lly based multiscale computational models of excitation-contraction coupling and the insights that ha

97 e findings enhance our understanding of both excitation-contraction coupling and the pathology of myo

98 uces the classic physiological properties of excitation-contraction coupling and, under pathophysiolo

99 sible role for cav-3 as a modifier of muscle excitation-contraction coupling and/or for localization

100 Direct effects of Ang-(1-9) on cardiomyocyte excitation/contraction coupling and cardiac contraction

101 gulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wi

102 ac myocyte markers, sarcomeric organization, excitation-contraction coupling, and action potentials c

103 (RyR) are key components of striated muscle excitation-contraction coupling, and alterations in thei

104 sses such as cardiomyocyte (CM) hypertrophy, excitation-contraction coupling, and apoptosis; non-CM-s

105 ributes to T-tubule disorganization, loss of excitation-contraction coupling, and heart failure devel

106 elease is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this releas

107 SC-CM, including lack of T-tubules, immature excitation-contraction coupling, and inefficient Ca-indu

108 release termination is important for stable excitation-contraction coupling, and partial [Ca(2+)](SR

109 sses including neuronal excitability, muscle excitation-contraction coupling, and secretion.

110 and control neuronal communication, cardiac excitation-contraction coupling, and skeletal muscle fun

111 it (CRU) is the fundamental event of cardiac excitation-contraction coupling, and spontaneous release

112 ves that occur within atrial myocytes during excitation-contraction coupling, and the effect of posit

113 n maintaining normal I(Ca), Ca(2+) handling, excitation-contraction coupling, and the in vivo heart f

114 ll is related to interspecies differences in excitation-contraction coupling, and we report the first

115 Despite this asynchronous form of excitation-contraction coupling, animals can actively re

116 ne receptor is an essential component of the excitation-contraction coupling apparatus.

117 Defects in excitation-contraction coupling are associated with musc

118 r to V(m) depolarization, suggesting reverse excitation-contraction coupling as their aetiology.

119 the junctional SR, which results in impaired excitation-contraction coupling at the level of the myoc

120 and RyR2(R4496C+/-) hearts, suggesting that excitation-contraction coupling between the sarcolemmal

121 ticulum (SR) Ca(2+) cycling is key to normal excitation-contraction coupling but may also contribute

122 the lack of triadin did not prevent skeletal excitation-contraction coupling but reduced the amplitud

123 iomyocytes, Ca(2+) is the central element of excitation-contraction coupling, but also impacts divers

124 These findings indicate that alterations in excitation-contraction coupling, but not in maximal SR-r

125 e-patterning is independent of their role in excitation-contraction coupling, but requires Ca(2+) inf

126 V1.1e variant functions as voltage sensor in excitation-contraction coupling, but unlike CaV1.1a it a

127 lar rhythmicity contributes significantly to excitation-contraction coupling by altering the expressi

128 ndrial contribution to Ca(2+) removal during excitation-contraction coupling by comparing Ca(2+) tran

129 We conclude that TRD enhances cardiac excitation-contraction coupling by directly stimulating

130 smic reticulum (SR) plays a critical role in excitation-contraction coupling by regulating the cytopl

131 We conclude that miR-1 enhances cardiac excitation-contraction coupling by selectively increasin

132 subunit plays a key role in skeletal muscle excitation-contraction coupling by sensing membrane volt

133 the membrane potential becomes higher during excitation-contraction coupling, Ca can enter through bo

134 this study, we report the influence of UN on excitation-contraction coupling, Ca(2+)-induced Ca(2+) r

135 confer MHS and promote basal disturbances of excitation-contraction coupling, [Ca(2+)](rest), and oxy

136 errant splicing of the pre-mRNA encoding the excitation-contraction coupling component Junctin.

137 Effective and stable excitation-contraction coupling critically depends not o

138 nt and both spontaneous and stimuli-elicited excitation-contraction coupling cycles appeared within 1

139 es responsible for sarcomere contraction and excitation-contraction coupling decreased by 43% +/- 4%

140 ase to sarcolemmal membranes, causing severe excitation-contraction coupling defects.

141 In cardiac myocytes, excitation-contraction coupling depends upon sarcoplasmi

142 Cardiac excitation-contraction coupling (EC coupling) links the

143 ntraction or relaxation, a process known as "excitation-contraction coupling" (EC-coupling).

144 voked by tonic neurostimulation, even though excitation contraction coupling (ECC) remains unperturbe

145 Ca2+ plays a pivotal role in both excitation-contraction coupling (ECC) and activation of

146 We studied excitation-contraction coupling (ECC) and inositol-1,4,5

147 but its potential to influence physiological excitation-contraction coupling (ECC) and muscle functio

148 plays an important role in the modulation of excitation-contraction coupling (ECC) in atrial tissue a

149 asmic reticulum (SR) Ca(2+) release mediates excitation-contraction coupling (ECC) in cardiac myocyte

150 the major Ca2+ release channel required for excitation-contraction coupling (ECC) in skeletal muscle

151 slate into functional effects during cardiac excitation-contraction coupling (ECC) is much less clear

152 CT: In atrial myocytes Ca(2+) release during excitation-contraction coupling (ECC) is strikingly diff

153 hole-cell [Ca2+]i transients observed during excitation-contraction coupling (ECC).

154 d by NaV1.5 mutants and propose that, during excitation-contraction coupling, elevated intracellular

155 es the function of many proteins involved in excitation-contraction coupling, elucidation of its role

156 verse facets of cardiac physiology including excitation-contraction coupling, excitability, and gene

157 dx skeletal muscle, which may play a role in excitation-contraction coupling failure and progression

158 act otherwise hidden fine details in cardiac excitation-contraction coupling from high-speed 2-dimens

159 yadic volume and reduced LCCs/RyR2s decrease excitation-contraction coupling gain and cause asynchron

160 g-protein, can have a dramatic effect on the excitation-contraction coupling gain and that this gain

161 in adult rat myocytes led to an increase in excitation-contraction coupling gain and to more frequen

162 , sarcoplasmic reticulum Ca(2+) release, and excitation-contraction coupling gain were also measured.

163 ), the amplitude of the Ca(2+) transient and excitation-contraction coupling gain, but, again, there

164 JPH2 deficiency resulted in loss of excitation-contraction coupling gain, precipitated by a

165 l protein, and macroscale phenomena, such as excitation-contraction coupling gain.

166 ions to RyR2 binding sites, thus increasing excitation-contraction coupling gain.

167 ducing either i(Ca) or NP(o) alone increased excitation-contraction coupling gain.

168 based SR Ca(2+) leak, and it produces normal excitation-contraction coupling gain.

169 The model predicts changes in excitation-contraction coupling 'gain' that result from

170 c II-III loop, essential for skeletal muscle excitation-contraction coupling, has been replaced with

171 ate sarcoplasmic reticulum Ca(2+) levels and excitation-contraction coupling; hence, TRP channels exp

172 RyR2-dependent Ca2+ release is critical for excitation-contraction coupling; however, a functional r

173 ent signaling in cardiac myocytes, including excitation-contraction coupling; however, the subcellula

174 ntegrated, with parallel signals controlling excitation-contraction coupling, hypertrophy, and metabo

175 l and intracellular membrane remodelling and excitation-contraction coupling; (ii) mitochondrial dist

176 rk provides a platform for future studies of excitation contraction coupling in skeletal muscle fiber

177 rmation on microscopic calcium signaling and excitation-contraction coupling in a robust manner.

178 molecular components sufficient to modulate excitation-contraction coupling in adult muscle fibers.

179 Excitation-contraction coupling in atrial cells is media

180 nce from the cytosol is essential for normal excitation-contraction coupling in both skeletal and car

181 rrents conducted by CaV1.2 channels initiate excitation-contraction coupling in cardiac and vascular

182 e receptor, RyR2) plays an essential role in excitation-contraction coupling in cardiac muscle cells.

183 the sarcoplasmic reticulum (SR) required for excitation-contraction coupling in cardiac muscle.

184 Excitation-contraction coupling in cardiac myocytes occu

185 annels (VDCCs) play a pivotal role in normal excitation-contraction coupling in cardiac myocytes.

186 ed by clusters of ryanodine receptors during excitation-contraction coupling in cardiac myocytes.

187 a(2+) channels of the Ca(V)1 family initiate excitation-contraction coupling in cardiac, smooth, and

188 g of structures and proteins associated with excitation-contraction coupling in cardiomyocytes in DHF

189 precise Ca(2+)-induced Ca(2+) release during excitation-contraction coupling in cardiomyocytes.

190 (I(Ca)) and calcium cycling, which disrupted excitation-contraction coupling in cardiomyocytes.

191 voltage-gated Ca(2+) channel CaV1.2 initiate excitation-contraction coupling in cardiomyocytes.

192 e results will help to explain remodeling of excitation-contraction coupling in disease and restorati

193 AT couplon "super-hubs" thus underlie faster excitation-contraction coupling in health as well as hyp

194 intracellular signaling cascades, including excitation-contraction coupling in heart.

195 ) by immunoaffinity column chromotography on excitation-contraction coupling in isolated myocytes.

196 similar, implying an increase in the gain of excitation-contraction coupling in KO cells.

197 mooth muscle-specific beta1 subunit regulate excitation-contraction coupling in many types of smooth

198 CNMs via defective membrane trafficking and excitation-contraction coupling in muscle.

199 al for numerous cellular functions including excitation-contraction coupling in muscle.

200 chemical evidence that Stac3 participates in excitation-contraction coupling in muscles.

201 P2 on bioenergetics, Ca(2+) homeostasis, and excitation-contraction coupling in neonatal cardiomyocyt

202 Ca(V)1 channels initiate excitation-contraction coupling in skeletal and cardiac

203 possible mechanisms underlying the impaired excitation-contraction coupling in skeletal muscle fibre

204 The molecular basis for excitation-contraction coupling in skeletal muscle is ge

205 ate a direct physiological role of S100A1 in excitation-contraction coupling in skeletal muscle.

206 ns constitute the key elements essential for excitation-contraction coupling in skeletal muscle.

207 through these channels is a critical step in excitation-contraction coupling in smooth muscle cells.

208 Excitation-contraction coupling in striated muscle requi

209 on of actin and myosin, effectively allowing excitation-contraction coupling in striated muscle.

210 itial description of regional differences in excitation-contraction coupling in the adult mouse heart

211 this structural organization is crucial for excitation-contraction coupling in the body wall muscle,

212 Excitation-contraction coupling in the cardiac myocyte i

213 ryanodine receptor 2 (RyR2) is required for excitation-contraction coupling in the heart and is also

214 Intracellular Ca is crucial for normal excitation-contraction coupling in the heart and plays a

215 Excitation-contraction coupling in the heart depends on

216 uniform Ca release that is characteristic of excitation-contraction coupling in the heart ventricle.

217 -gated calcium channel 1.2 (CaV1.2) initiate excitation-contraction coupling in the heart, and altere

218 (RyR2)/calcium release channel, required for excitation-contraction coupling in the heart, has been l

219 calcium release channel (RyR2), required for excitation-contraction coupling in the heart, is abundan

220 rrents conducted by CaV1.2 channels initiate excitation-contraction coupling in the heart.

221 age-gated Ca(2+) channel, Ca(v)1.2, mediates excitation-contraction coupling in the heart.

222 alterations of several proteins involved in excitation-contraction coupling in the ob/ob mice, inclu

223 ficked to the membrane, and supported robust excitation-contraction coupling in the presence of nisol

224 MKII, and CaN with the Shannon-Bers model of excitation-contraction coupling in the rabbit ventricula

225 f a requirement for these channels in normal excitation-contraction coupling in ventricular myocytes.

226 n CNM2 by disrupting machinery necessary for excitation-contraction coupling in vertebrate organisms.

227 Skeletal muscle excitation-contraction coupling involves activation of h

228 In skeletal muscle, excitation-contraction coupling involves the activation

229 Cardiac excitation-contraction coupling is a highly coordinated

230 its participation in the trigger process of excitation-contraction coupling is controversial.

231 Cardiac excitation-contraction coupling is initialized by the re

232 preciation of spatiotemporal fine details of excitation-contraction coupling is instrumental for the

233 tion to SR Ca(2+) storage and release during excitation-contraction coupling is largely dispensable.

234 tion of many of the key proteins involved in excitation-contraction coupling is located predominantly

235 remodeling and cellular signaling, even when excitation-contraction coupling is present.

236 +], a realistic but minimal model of cardiac excitation-contraction coupling is produced.

237 KEY POINTS: In atrial myocytes excitation-contraction coupling is strikingly different

238 Excitation-contraction coupling is the bridge between ca

239 alcium channel that controls skeletal muscle excitation-contraction coupling, is markedly repressed i

240 ch are consistent with the idea that cardiac excitation-contraction coupling largely occurs at the T-

241 Here we present a computational model of excitation-contraction coupling linked to mitochondrial

242 nown to influence muscle contraction through excitation contraction coupling, little is understood of

243 Thus, the excitation-contraction coupling machinery of both iPS- a

244 e identify Stac3 as a novel component of the excitation-contraction coupling machinery.

245 gest a host of potential mechanisms by which excitation-contraction coupling may also be modulated.

246 sults can be explained if non-linearities in excitation-contraction coupling mechanisms modify the co

247 ocyte offers a direct means of understanding excitation-contraction coupling mechanisms.

248 t postshock early site suggests that reverse excitation-contraction coupling might be responsible for

249 These RyR2s could contribute to excitation-contraction coupling, mitochondrial and nucle

250 ic changes orchestrate cardiac architecture, excitation-contraction coupling, mitochondrial biogenesi

251 on incorporating cellular electrophysiology, excitation-contraction coupling, mitochondrial energetic

252 ncluding action potentials and arrhythmias), excitation-contraction coupling, modulation of contracti

253 During excitation-contraction coupling, most Ca sparks are indu

254 hannels play a key role in initiating muscle excitation-contraction coupling, neurotransmitter releas

255 myocytes are critical microdomains, in which excitation-contraction coupling occurs.

256 myocytes are critical microdomains, in which excitation-contraction coupling occurs.

257 ould promote T-tubule development and mature excitation-contraction coupling of hiPSC-CM when culture

258 2+) channels that play a pivotal role in the excitation-contraction coupling of skeletal and cardiac

259 iews the potential roles of calsequestrin in excitation-contraction coupling of skeletal muscle.

260 f-state and result in excessively sensitized excitation-contraction coupling of the contractile appar

261 ry pathogenic abnormality involves defective excitation-contraction coupling, other abnormalities lik

262 ut it remains unknown whether all SFMs share excitation-contraction coupling pathway adaptations for

263 plays a significant role in skeletal muscle excitation-contraction coupling, primarily through speci

264 ining normal arterial tone by regulating the excitation-contraction coupling process.

265 arlo approaches to modeling local control of excitation-contraction coupling produce high-gain Ca2+ r

266 sure approach to simulating local control of excitation-contraction coupling produces high-gain Ca2+

267 Here, we review how normal and abnormal excitation-contraction coupling properties emerge from t

268 direct effect of PSEN1 sequence variants on excitation-contraction coupling protein function.

269 f the Na(+)/Ca(2+) exchanger, although other excitation-contraction coupling protein levels were not

270 d protein gels reveal that the expression of excitation-contraction coupling proteins is enhanced in

271 prolonged loss jeopardizes bioenergetics and excitation-contraction coupling, providing a potential p

272 ylation contribute to dysfunction of cardiac excitation-contraction coupling remains controversial.

273 ulation of neuronal excitability and cardiac excitation-contraction coupling requires the proper loca

274 to a substantially reduced energy supply for excitation-contraction coupling resulting from a lower f

275 is maintained by an increase in the gain of excitation-contraction coupling resulting from both a mo

276 e by depressing RyR2 channel activity during excitation-contraction coupling, resulting in random bur

277 cardiac action potential and has a critical excitation-contraction coupling role.

278 d Ca(2+) transients from thousands of active excitation-contraction coupling sites (ECC couplons) com

279 ts at multiple subcellular sites involved in excitation contraction coupling, such as decreasing memb

280 PMCA) extrudes Ca2+ but has little effect on excitation-contraction coupling, suggesting its potentia

281 diac ventricular myocytes, events crucial to excitation-contraction coupling take place in spatially

282 gets, particularly those involved in cardiac excitation-contraction coupling, that may prove to be at

283 Beginning with the fundamental unit of excitation-contraction coupling, the couplon where L-typ

284 Excitation-contraction coupling, the process that regula

285 is shares many ion flux pathways with normal excitation-contraction coupling, the role of the t-tubul

286 ation and depletion in t-system lumen during excitation-contraction coupling to ensure effective loca

287 model of the beta(1)-adrenergic pathway and excitation-contraction coupling to include detailed rece

288 ctivation of calcium channels by restricting excitation-contraction coupling to more negative voltage

289 ultiple functional adaptations that minimize excitation-contraction coupling transduction times.

290 ossible contribution of TTX-sensitive INa to excitation-contraction coupling, using 200 nmol/L TTX to

291 model of the cardiac myocyte that describes excitation-contraction coupling via stochastic simulatio

292 Although operational excitation-contraction coupling was demonstrable in the

293 the ability of the mutant channel to engage excitation-contraction coupling was largely unaffected b

294 +], a realistic but minimal model of cardiac excitation-contraction coupling was produced that avoids

295 Myocyte contractility, Ca(2+) handling and excitation-contraction coupling were studied in isolated

296 coplasmic reticulum (SR) and are critical in excitation-contraction coupling, whereas the inositol tr

297 s an alteration in ventricular cardiomyocyte excitation-contraction coupling which contributes to the

298 ey proteins involved in Ca(2+) signaling and excitation-contraction coupling, which are known to be e

299 cts on beat-to-beat [Ca(2+)](c) handling and excitation-contraction coupling, which may contribute to

300 matical model of the cardiac cell that links excitation-contraction coupling with mitochondrial energ