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 ver the full range of voltage sensitivity of EC coupling.

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

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

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

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

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

9 ir functional defects and how they influence EC coupling.

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

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

12 contribute to the activation of RyR1 during EC coupling.

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

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

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

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

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

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

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

20 hat presumably represent functional sites of EC coupling.

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

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

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

24 oskeletal defects that reflect a blockade of EC coupling.

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

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

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

28 performs vital functions not associated with EC coupling.

29 activators and do not support skeletal type EC coupling.

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

31 ward potassium current, alters properties of EC coupling.

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

33 in alpha1S that influence the efficiency of EC coupling.

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

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

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

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

38 n fish by disrupting 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 e in skeletal muscle excitation-contraction (EC) coupling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 3 was identified as an essential protein for EC coupling and is part of a group of three proteins tha

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

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

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

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

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

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

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

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

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

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

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

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

75 (2+) released during excitation-contraction (EC) coupling, and defects in EC coupling are associated

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

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

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

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

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

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

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

83 (1S) III-IV loop is not directly involved in EC coupling but does influence DHPR gating transitions i

84 1 functions not only to activate RyR1 during EC coupling, but also to suppress resting RyR1-mediated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 8A/V485A/V492A) recovered weak skeletal-type EC coupling (DeltaF/F(max) = 0.4 +/- 0.1 vs. 2.7 +/- 0.5

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 EC coupling requires communication between voltage-sensi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 EC coupling was found to be weakened in myotubes express

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

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

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

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

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

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

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