ライフサイエンスコーパス: EC coupling

1 modulating excitation-contraction coupling (EC coupling).

2 known as "excitation-contraction coupling" (EC-coupling).

3 s for phenotypic expression of skeletal-type EC coupling.

4 ward potassium current, alters properties of EC coupling.

5 ce-voltage curve indicative of skeletal-type EC coupling.

6 in alpha1S that influence the efficiency of EC coupling.

7 gating and the role of dyad configuration on EC coupling.

8 ed domain D4, is essential for skeletal-type EC coupling.

9 is essential for expression of skeletal-type EC coupling.

10 type 1 (RyR1) important for skeletal muscle EC coupling.

11 receptor are needed in order to allow normal EC coupling.

12 ir functional defects and how they influence EC coupling.

13 Ca2+ influx is unnecessary for skeletal-type EC coupling.

14 he skeletal III-IV domain in the recovery of EC coupling.

15 contribute to the activation of RyR1 during EC coupling.

16 t differ from RyR1 in its ability to mediate EC coupling.

17 aR16 was found to mediate weak skeletal-type EC coupling.

18 P3Rs, and that these channels could modulate EC coupling.

19 rdless of the participation of these RyRs in EC coupling.

20 ration of charge movements and skeletal-type EC coupling.

21 a low density of charge movements, and lack EC coupling.

22 hat presumably represent functional sites of EC coupling.

23 ver the full range of voltage sensitivity of EC coupling.

24 1 interaction, essential for skeletal muscle EC coupling.

25 ds of beta1a, which are essential to support EC coupling.

26 Ca(2+) currents but only marginally restored EC coupling.

27 ution of Ca(2+)-gated ryanodine receptors to EC coupling.

28 Stac3 in skeletal muscle causes the loss of EC coupling.

29 R/RyR1 signaling that supports skeletal-type EC coupling.

30 oskeletal defects that reflect a blockade of EC coupling.

31 a(1a) subunits of the DHPR are essential for EC coupling.

32 ated the L-type current and had no effect on EC coupling.

33 nd Ca(2+) release channel in skeletal muscle EC coupling.

34 performs vital functions not associated with EC coupling.

35 activators and do not support skeletal type EC coupling.

36 lcium regulation and excitation-contraction (EC) coupling.

37 to the mechanism of excitation-contraction (EC) coupling.

38 for skeletal muscle excitation-contraction (EC) coupling.

39 d for cardiac muscle excitation-contraction (EC) coupling.

40 d voltage sensor for excitation-contraction (EC) coupling.

41 odulation of cardiac excitation-contraction (EC) coupling.

42 and is required for excitation-contraction (EC) coupling.

43 for skeletal muscle excitation-contraction (EC) coupling.

44 because of defective excitation-contraction (EC) coupling.

45 n fish by disrupting excitation-contraction (EC) coupling.

46 e in skeletal muscle excitation-contraction (EC) coupling.

47 he myocardium and to excitation-contraction (EC) coupling.

48 so modulates cardiac excitation-contraction (EC) coupling.

49 tor (RyR1) underlies excitation-contraction (EC) coupling.

50 e voltage sensor for excitation-contraction (EC) coupling.

51 S to RyR1 to trigger excitation-contraction (EC) coupling.

52 To test for Ca(2+)-entry independent EC coupling, a pore mutation (E1014K) known to entirely

53 tion underlie differences in [Ca(2+)](i) and EC coupling across the left ventricular free wall.

54 required for cardiac excitation-contraction (EC) coupling, activating the RyR2 channel, and increasin

55 re, a heptad repeat in beta1aD5 controls the EC coupling activity.

56 he D2 domain of RyR1 plays a key role during EC coupling, additional region(s) from the N-terminal en

57 we examined whether a cardiac muscle type of EC coupling also mediates contraction in this tissue.

58 cardiac inotropy and enhanced efficiency of EC coupling alternans is less likely to occur.

59 e DHPR gating transitions important both for EC coupling and activation of L-type conductance.

60 Calcium channels are major players of EC coupling and are regulated by voltage and Ca(2+)/calm

61 These differences in EC coupling and beta-adrenergic sensitivity may help exp

62 residues 851-896) of GFP-SkLC restored both EC coupling and Ca(2+) current densities like those of t

63 eduction of voltage-dependent, skeletal-type EC coupling and emergence of Ca2+ transients triggered b

64 myotubes expressing GFP-SkLC or SkLC lacked EC coupling and had very small Ca(2+) currents.

65 ovide insights into the energetic demands of EC coupling and highlight the dynamic nature of ATP conc

66 findings define critical roles for Stac3 in EC coupling and human disease.

67 3 was identified as an essential protein for EC coupling and is part of a group of three proteins tha

68 as occurs during heart failure) destabilizes EC coupling and may lead to sudden cardiac death.

69 tioning of the DHPR, including skeletal-type EC coupling and retrograde signaling.

70 We identified differential abnormalities in EC coupling and ryanodine receptor disruption in flexor

71 ains a motif required for both skeletal-type EC coupling and RyR-1-mediated enhancement of Ca(2+) cur

72 ryanodine, indicated a loss of skeletal-type EC coupling and the emergence of an EC coupling componen

73 re due to increased SR Ca(2+) release during EC coupling and to physiological hypertrophy, but not to

74 of dysferlin alone preserved sensitivity for EC coupling and was associated with larger ryanodine rec

75 oduces experimentally measured properties of EC coupling and whole cell phenomena.

76 t have been characterized previously augment EC coupling and/or increase the rate of L-type Ca(2+) en

77 integrated model of excitation-contraction (EC) coupling and mitochondrial energetics (ECME model) i

78 and HFpEF to compare excitation-contraction (EC) coupling and protein expression in these two forms o

79 In skeletal muscle, excitation-contraction (EC) coupling and retrograde signaling are thought to res

80 if for skeletal-type excitation-contraction (EC) coupling and retrograde signaling in vivo.

81 a loss of dysferlin reduced sensitivity for EC coupling, and produced disorganized and smaller ryano

82 the heart, whereby Na(V)1.6 participates in EC coupling, and represents an intrinsic depolarizing re

83 induces a conformation change that disrupts EC coupling, and this conformational change is partially

84 (2+) released during excitation-contraction (EC) coupling, and defects in EC coupling are associated

85 were used to examine excitation-contraction (EC) coupling, and the relation between the plasma membra

86 h domain 3) is an essential component of the EC coupling apparatus and a mutation in human STAC3 caus

87 on-contraction (EC) coupling, and defects in EC coupling are associated with human myopathies.

88 responsible for the excitation-contraction (EC) coupling are exclusively localized in specific retic

89 in the membrane functioned as efficiently in EC coupling as GFP-alpha(1S).

90 he scrambled DHPR also rescued skeletal-type EC coupling, as indicated by electrically evoked contrac

91 While HFrEF is characterized by defective EC coupling at baseline, HFpEF exhibits enhanced couplin

92 together confirm a critical role of STAC3 in EC coupling but also suggest that STAC3 may have additio

93 te direct beta1a-RyR1 interactions, weakened EC coupling but did not replicate the truncated phenotyp

94 (1S) III-IV loop is not directly involved in EC coupling but does influence DHPR gating transitions i

95 1 functions not only to activate RyR1 during EC coupling, but also to suppress resting RyR1-mediated

96 in the II-III loop perturbs skeletal muscle EC coupling, but preserves the ability of STAC3 to slow

97 f CICR are able to reconstruct properties of EC coupling, but require computationally demanding stoch

98 hat Rem negatively regulates skeletal muscle EC coupling by reducing the number of functional L-type

99 cardiac myocytes, and that beta2AR* enhances EC coupling by reinforcing SR Ca2+ cycling (release and

100 Phenotypic expression of skeletal-type EC coupling by RyR1 with mutations in the K(3495)KKRR_ _

101 odulation of cardiac excitation-contraction (EC) coupling by beta-adrenergic receptor (beta-AR) stimu

102 myotubes fully restored Ca(2+) currents and EC coupling Ca(2+) release, whereas expression of Stac3W

103 not generate appreciable Ca(2+) currents or EC coupling Ca(2+) release.

104 ght to underlie both excitation-contraction (EC) coupling Ca(2+) release from the SR and retrograde c

105 with previously validated models of cardiac EC coupling, Ca(2+)/calmodulin-dependent activation of C

106 We conclude that potentiation of EC coupling can be correlated with both [Ca](SRT) and [C

107 ssed in non-muscle cells, their influence on EC coupling can only be studied in skeletal myotubes.

108 tal-type EC coupling and the emergence of an EC coupling component triggered by the Ca(2+) current.

109 Excitation-contraction (EC) coupling comprises events in muscle that convert ele

110 8A/V485A/V492A) recovered weak skeletal-type EC coupling (DeltaF/F(max) = 0.4 +/- 0.1 vs. 2.7 +/- 0.5

111 Consequently, beta3 failed to restore EC coupling despite the fact that both beta3 and beta1a

112 tal pore subunit alpha1S, overrides critical EC coupling determinants present in alpha1S.

113 conduction pathways, excitation-contraction (EC) coupling, development and stress responses.

114 e, we investigated the mechanisms underlying EC coupling differences between mouse left ventricular e

115 Fundamental differences in EC coupling distinguish HFrEF from HFpEF.

116 It is unknown whether EC coupling domains present in the beta-subunit influenc

117 The low skeletal-type EC coupling expressed by the alpha1C/alpha1S II-III loop

118 Recent work has shown that EC coupling fails in muscle from mice and fish null for

119 However, the mechanism leading to EC coupling failure remains unclear.

120 scle ultrastructure, excitation-contraction (EC) coupling, fibre type, and expression of other Ca(2)(

121 es in key regulatory events required for the EC coupling function of the DHPR.

122 region, which confer excitation-contraction (EC) coupling function to chimeric dihydropyridine recept

123 ncy-dependent acceleration of relaxation and EC coupling gain (which was highly sarcoplasmic reticulu

124 uggest that the characteristic steep rise in EC coupling gain observed at hyperpolarized potentials i

125 +) transients remained unchanged because the EC coupling gain was up-regulated by an increased neuroe

126 al for skeletal-type excitation-contraction (EC) coupling have been described in the cytosolic loops

127 esult of periodic alterations in the gain of EC coupling, i.e. the efficacy of a given trigger signal

128 f and Fer myofibers and slightly potentiated EC coupling in Dysf myofibers.

129 lity of RyR1/RyR3 chimera to rescue skeletal EC coupling in dyspedic myotubes.

130 These data reveal impaired EC coupling in Myof and Fer myofibers and slightly poten

131 ze the role of SR Ca2+ release during normal EC coupling in NB ventricular myocytes.

132 These findings indicate that EC coupling in skeletal muscle involves the interplay of

133 ry for the initiation of Ca2+ release during EC coupling in skeletal muscle.

134 rs to contribute to but is not essential for EC coupling in skeletal muscle.

135 ctional voltage sensor capable of triggering EC coupling in skeletal myotubes can be recovered by the

136 HPR beta1a subunit in fast voltage dependent EC coupling in skeletal myotubes.

137 diadic junctions in excitation-contraction (EC) coupling in adult (AD) ventricular myocytes suggests

138 al control theory of excitation-contraction (EC) coupling in cardiac muscle asserts that L-type Ca(2+

139 ristic properties of excitation-contraction (EC) coupling in cardiac myocytes, such as high gain and

140 ading to failures of excitation-contraction (EC) coupling in central regions of the cell.

141 (SR) Ca2+-ATPase on excitation-contraction (EC) coupling in guinea-pig ureter, by measuring membrane

142 a(2+) release during excitation-contraction (EC) coupling in muscle.

143 otein that modulates excitation-contraction (EC) coupling in skeletal and cardiac muscle.

144 Excitation-contraction (EC) coupling in skeletal muscle depends upon trafficking

145 Excitation-contraction (EC) coupling in skeletal muscle requires a physical inte

146 Excitation-contraction (EC) coupling in skeletal muscle requires functional and

147 protein complex for excitation-contraction (EC) coupling in skeletal muscle.

148 yRs are required for excitation-contraction (EC) coupling in striated (cardiac and skeletal) muscles.

149 oteins essential for excitation-contraction (EC) coupling in striated muscle.

150 Excitation-contraction (EC) coupling in striated muscles is mediated by the card

151 ads, we now assessed excitation contraction (EC) coupling in these models.

152 ionally relevant for excitation-contraction (EC) coupling in vivo, we have studied the ability of RyR

153 ve shown that the same signals that regulate EC-coupling in SMCs are also capable of regulating SMC-s

154 omplex (required for excitation-contraction [EC] coupling in heart muscle).

155 ytes from rats with HFrEF exhibited impaired EC coupling, including decreased Ca(2+) transient (CaT)

156 trast, HFpEF cardiomyocytes showed saturated EC coupling (increased I(Ca) , high probability of coupl

157 It is suggested that the efficiency of EC coupling is locally controlled in the microenvironmen

158 The data strongly suggest that skeletal-type EC coupling is not uniquely controlled by alpha(1S) 720-

159 molecular mechanism that initiates skeletal EC coupling is unresolved, it is clear that both the alp

160 Excitation-contraction (EC) coupling is altered in end-stage heart failure.

161 eptor participate in excitation-contraction (EC) coupling is critical to validate current structural

162 lthough DHPR Ca(2+) influx is irrelevant for EC coupling, its putative role in other muscle-physiolog

163 e present defects in excitation-contraction (EC) coupling likely responsible for the disease-associat

164 Cardiac excitation-contraction coupling (EC coupling) links the electrical excitation of the cell

165 haracterized, but required, component of the EC coupling machinery of skeletal muscle and introduce a

166 of genes encoding specific components of the EC coupling machinery suggests that crude oil disrupts e

167 Collectively, our data implicate that EC-coupling mechanisms in striated muscles may also broa

168 protein assays suggest that these changes in EC coupling mode are not due to shifts in dihydropyridin

169 These results indicate that a change in EC coupling mode occurs in a population of fibres in age

170 e whether changes in excitation-contraction (EC) coupling mode occur in skeletal muscles from ageing

171 unction in HF, suggesting that a generalized EC coupling myopathy may play a role in HF.

172 FP-alpha1A and GFP-alpha1B failed to restore EC coupling of any type.

173 quantified the contribution to skeletal-type EC coupling of the alpha1S (CaV1.1) II-III loop when alo

174 on Ca2+ handling and excitation-contraction (EC) coupling of MH-only and MH + CCD mutations in RyR1 a

175 geing mammals by examining the dependence of EC coupling on extracellular Ca(2+).

176 ing the role of the alpha2/delta1 subunit in EC coupling or in other cell functions.

177 that RyR3, although incapable of supporting EC coupling or tetrad formation, restored a significant

178 a2+ activation amplifies Ca2+ release during EC coupling, or that the E4032A mutation generally inhib

179 part, skeletal-type excitation-contraction (EC) coupling (orthograde signaling) but failed to enhanc

180 ewborn (NB) cells may manifest as an altered EC coupling phenotype.

181 or the skeletal-type excitation-contraction (EC) coupling phenotype.

182 necessary for a quantitative recovery of the EC-coupling phenotype of skeletal myotubes.

183 membrane protein of the SR unrelated to the EC coupling process.

184 ates, driven by an electrochemical-chemical (EC) coupling process, and that geometric changes in the

185 KO and RyR1 KO myotubes, the Ca2+-dependent EC coupling promoted by beta2a overexpression had the fo

186 The loss in voltage-dependent EC coupling promoted by beta2a was inferred by the drast

187 mulation incorporates details of microscopic EC coupling properties in the form of Ca(2+) release uni

188 otting and PCR were used to assay changes in EC coupling protein and RNA expression.

189 ated the swimming behavior and expression of EC coupling proteins in larval fathead minnows (Pimephal

190 /beta1a 325-524) recapitulates skeletal-type EC coupling quantitatively and was used to generate trun

191 III-IV loop alter the voltage dependence of EC coupling, raising the possibility that this loop is d

192 EC coupling requires communication between voltage-sensi

193 ically enhanced the formation of tetrads and EC coupling rescue by constructs that otherwise are only

194 al- and cardiac-type excitation-contraction (EC) coupling, respectively, whereas expression of GFP-al

195 region resulted in a dramatic enhancement of EC coupling restored by an RyR3 chimera containing amino

196 Skeletal muscle excitation-contraction (EC) coupling roots in Ca(2+)-influx-independent inter-ch

197 not the alpha1S-subunit alone, controls the EC coupling signal in skeletal muscle.

198 o address this question, we investigated the EC coupling signal that is generated when the endogenous

199 an reproduce both the detailed properties of EC coupling, such as variable gain and graded SR Ca(2+)

200 Thus, the same defect in EC coupling that develops during hypertrophy may contrib

201 the C-terminal tail of the voltage sensor of EC coupling, the dihydropyridine receptor.

202 sensor that triggers excitation-contraction (EC) coupling, the four-domain pore subunit of the dihydr

203 roteins critical for excitation-contraction (EC) coupling, the type 1 ryanodine receptor (RyR1) and C

204 apable of transferring strong, skeletal-type EC coupling to an otherwise cardiac DHPR.

205 domain by itself failed to restore skeletal EC coupling to RyR3, the addition of the D2 region resul

206 During normal skeletal muscle EC coupling, transverse (t) tubule depolarization trigge

207 taF/F versus voltage curve, and emergence of EC coupling triggered by the Ca(2+) current.

208 d voltage sensor for excitation-contraction (EC) coupling, triggering Ca(2+) release via the type 1 r

209 a(2+) release during excitation-contraction (EC) coupling varies across the left ventricular free wal

210 EC coupling was found to be weakened in myotubes express

211 This impaired EC coupling was not a consequence of altered function of

212 When fragments were expressed separately, EC coupling was not recovered.

213 ed SR Ca(2+) release, the "gain" function of EC coupling was uncompromised, and SR Ca(2+) content, di

214 Excitation-contraction (EC) coupling was characterized with respect to both gain

215 ecessary for the initiation of skeletal-type EC coupling, we examined the behavior of RyR1 with gluta

216 ify the role of the alpha(1S) III-IV loop in EC coupling, we examined the functional properties of a

217 e aforementioned beta2AR* effects on cardiac EC coupling without affecting the sarcolemmal ICa.