ライフサイエンスコーパス: T tubule

1 cardiac myocytes lacking transverse tubules (t-tubules).

2 olocalization in cardiac transverse tubules (T-tubules).

3 T-1 receptors in cardiac transverse tubules (T-tubules).

4 a2+ cycling appear to be concentrated at the t-tubule.

5 iomyocyte size, and development of extensive T tubules.

6 h most exhibiting an abnormal orientation of T tubules.

7 ng voltage-gated calcium channels located in T tubules.

8 f sodium channels close to the mouths of the T tubules.

9 ustered selectively around the mouths of the T tubules.

10 ll T-tubule systems, and averaged spacing of T-tubules.

11 invaginations of the cell membrane known as t-tubules.

12 bules (t-tubules), while NHE1 is absent from t-tubules.

13 Ca(2+) release in cardiac myocytes that lack t-tubules.

14 es but an increased presence of longitudinal T-tubules.

15 0% reduction in the contacts between jSR and T-tubules.

16 by translocation of GLUT4 to sarcolemma and T-tubules.

17 ecting delayed disappearance of insulin from t-tubules.

18 perinuclear depots and sarcolemma but not at t-tubules.

19 intracellular compartments to sarcolemma and t-tubules.

20 lar vesicles, the latter closely allied with T-tubules.

21 tercalated disks but was not detected at the t-tubules.

22 ed with dAmph postsynaptically and at muscle T-tubules.

23 omplexes preferentially localized in cardiac T-tubules.

24 t on Ca2+ efflux in atrial cells, which lack t-tubules.

25 em, with dilated and longitudinally oriented T-tubules.

26 lasmic reticulum apposing CaV1.2 channels at t-tubules.

27 ricular myocytes, LTCCs primarily cluster in T-tubules.

28 use, and fast approach for analyzing myocyte T-tubules.

29 at Ca(2+) extrusion systems are localized in T-tubules.

30 ed to 448 +/- 172 nm (mean +/- SD, number of t-tubules 348, number of cross sections 5323).

31 3D reconstructions of the t-tubules also suggested that some of them progressed fr

32 Tint), which provides a global evaluation of T-tubule alterations.

33 Epac1 were differentially concentrated along T tubules and around the nucleus, respectively.

34 r signaling, whereas Epac2 is located at the T tubules and regulates arrhythmogenic sarcoplasmic reti

35 a profound disruption to the openings of the t tubules and the cell surface in unloaded cardiomyocyte

36 ss of the orderly disposition of transverse (T)-tubules and a decrease of their associations with the

37 out (KO) mice and investigated cardiomyocyte t-tubule and cell structure and CICR over time and follo

38 The specialized T-tubule and costameric structures facilitate spatial co

39 tial for stabilizing the close apposition of T-tubule and sarcoplasmic reticulum membranes to form ju

40 ractional dye fluorescence (DeltaF/F) at the t-tubule and surface membranes of in situ mouse ventricu

41 lamp showed that LTCCs distribute equally in T-tubules and crest areas of the sarcolemma, whereas, in

42 exchanger (NCX) and Na/K-ATPase between the t-tubules and external sarcolemma.

43 malian heart are differentially localized to t-tubules and intercalated disks.

44 for particles </=11 nm; 2), the gaps between T-tubules and junctional sarcoplasmic reticulum (jSR), j

45 The possible presence of vestigial t-tubules and larger Ca(2+) content of central sarcoplas

46 tputs the densities of transversely oriented T-tubules and longitudinally oriented T-tubules, power s

47 onsistent H-zones, I-bands, and evidence for T-tubules and M-bands.

48 talized in muscle and primarily localized to T-tubules and not sarcolemma during insulin resistance.

49 ), cardiomyocytes showed progressive loss of t-tubules and remodelling of the cell surface, with prol

50 Half of AMs possessed T-tubules and structured topography, proportional to cel

51 act rat ventricular myocytes (i.e., from the T-tubules and surface sarcolemma) and in detubulated myo

52 tochemistry reveals KChIP2 expression in the t-tubules and the nucleus.

53 ease in the junctional coupling area between T-tubules and the SR and an elevated expression of the N

54 of myocytes in the left atrium had organized T-tubules and topography than in the right atrium.

55 urface, as in other tissues, but also within T-tubules and ultimately surrounding every mitochondrion

56 in their original position at sarcolemma or t-tubules and were locally depleted of GLUT4 by budding

57 layer-deforming properties of amphiphysin at T-tubules and, more generally, a physiological role of a

58 s of the sarcolemma (surface membrane versus T-tubules) and that Ca(2+) influx through these channels

59 cle EHD1 localizes to the transverse tubule (T-tubule), and loss of EHD1 results in overgrowth of T-t

60 cluding axon initial segments, cardiomyocyte T-tubules, and epithelial cell lateral membranes.

61 al basolateral membrane identity localize to T-tubules, and knockdown of AP-1gamma, required for baso

62 no longer associates with caveolin 3 in the T-tubules, and noncaveolin 3-associated calcium channels

63 ux by this mechanism, is concentrated in the t-tubules, and that the concentration of Ca2+ flux pathw

64 olonged exposure to ET-1; 2) degeneration of T-tubules; and 3) therapies targeted at erbB2 inhibition

65 Cardiomyocyte T tubules are important for regulating ion flux.

66 s study provides the first evidence that the T-tubules are a key site for the regulation of action po

67 These data suggest that the t-tubules are a key site for the regulation of transsarc

68 Thus, the t-tubules are an important determinant of cardiac cell f

69 ested that the structure and function of the t-tubules are more complex than previously believed; in

70 T-tubules are rich in L-type calcium channels, therefore

71 Transverse tubules (t-tubules) are uniquely-adapted membrane invaginations i

72 Furthermore, after photobleaching of t-tubule areas, recovery of GLUT4 was slow or absent, in

73 acent (1 microm) or more distant (20 microm) t-tubule areas.

74 ractant changes from all muscle membranes to T-tubules as invasion begins.

75 is approach is flawed because the density of T-tubules as well as non-T-tubule signals in the images

76 Cav-3 in both sarcolemmal and intracellular T-tubule-associated regions indicates the existence of m

77 ated a maintained organization of transverse T-tubules but an increased presence of longitudinal T-tu

78 ude that neuronal INa is concentrated at the t-tubules, but there is no evidence of a requirement for

79 initiation of propagated activity within the T tubules, by the triggering of the sodium channels clus

80 riggered by Ca(2+) entering the cell via the T-tubules (Ca(2+)-induced Ca(2+) release).

81 s depolarization events occurring in failing T-tubules can trigger local Ca(2+) release, resulting in

82 internalized to basal stores with a delay in t-tubules compared with sarcolemma, probably reflecting

83 lized with ryanodine receptor 2 (RyR2) in CM T-tubules, complexed with RyR2 in human and rat heart, a

84 y counteracts the well-characterized loss of t-tubule complexity and reduced expression of anchoring

85 In cardiac myocytes, T-tubules confer the necessary compartmentation of Ca(2+

86 ata showed that the newly grown longitudinal T-tubules contained Na(+)/Ca(2+)-exchanger proximal to r

87 etween junctional sarcoplasmic reticulum and T tubules (couplons), and of junctional sarcoplasmic ret

88 cantly reduces eccentric contraction-induced t-tubule damage, inflammation, and necrosis, which resul

89 m 3-month-old KO (3mKO), there were isolated t-tubule defects and Ca(2+) transient dysynchrony withou

90 myocardial infarction) in rats resulted in a T-tubule degradation (by approximately 40%) and signific

91 In rat, ferret, and sheep hearts t-tubule density and AmpII protein levels were lower in

92 T-tubule density was assessed by di-4-ANEPPS, FM4-64 or

93 In both HF models, AmpII protein and t-tubule density were decreased in the ventricles.

94 ntricular myocytes of large mammals with low T-tubule density, a significant number of ryanodine rece

95 ling rat hearts and measured z-groove index, T-tubule density, and compartmentalized beta(2)AR-mediat

96 This resulted from increased T-tubule density, as revealed by confocal images.

97 A-induced knockdown of AmpII protein reduced t-tubule density, calcium transient amplitude, and the s

98 Reducing AmpII protein decreases t-tubule density, reduces the amplitude, and increases t

99 morphology, quantified by z-groove index and T-tubule density, was normalized in reverse-remodeled he

100 s with reduced transient outward current and T-tubule density.

101 mal skeletal muscle EC coupling, transverse (t) tubule depolarization triggers sarcoplasmic reticulum

102 (a) Upon T-tubule depolarization a portion of the DHP receptor co

103 an interface the A-site is located), or (b) T-tubule depolarization may produce a local conformation

104 and Ca(2+) release); peptide C also blocked T-tubule depolarization-induced Ca(2+) release.

105 increased with the increase in the degree of T-tubule depolarization.

106 addition to standard protocols would promote T-tubule development and mature excitation-contraction c

107 tion on Matrigel mattress, is sufficient for T-tubule development, enhanced Ca-induced Ca release, an

108 Our novel findings, including T-tubule dilatation and disorganization, associated with

109 JP2 overexpression attenuates stress-induced T-tubule disorganization and protects against heart fail

110 arction mice was associated with progressive t-tubule disorganization, as quantified by fast-Fourier

111 e that down-regulation of JP2 contributes to T-tubule disorganization, loss of excitation-contraction

112 ially offsets the desynchronizing effects of t-tubule disruption in heart failure.

113 2+) release synchrony has been attributed to t-tubule disruption, but it is unknown if other factors

114 emoval of extracellular Ca(2+) or reduced by t-tubule disruption, in both genotypes.

115 is a structural protein responsible for jSR/T-tubule docking.

116 ammals or large mammals that have lost their t-tubules due to disease-induced structural remodeling (

117 n-contraction coupling largely occurs at the T-tubule dyadic clefts.

118 owledge are the first direct measurements of t-tubule electrical activity in ventricular cardiomyocyt

119 ty to intracellular ryanodine receptors, the t-tubules enable synchronous Ca(2+) release throughout t

120 r platelet production and muscle transverse (T) tubules facilitate excitation:contraction coupling.

121 In HF cardiomyocytes, sites where T-tubules fail to conduct AP show a slower and reduced l

122 In mice with cardiac Bin1 deletion, T-tubule folding is decreased, which does not change ove

123 ilizes dAmph in muscles, leading to impaired T-tubule formation and muscle function.

124 t led to disappearance of dAmph and impaired T-tubule formation, phenocopying amph-null mutants.

125 Notably, Matrigel mattress was necessary for T-tubule formation.

126 ed to affect muscle cell differentiation and T-tubule formation.

127 nly in the cell midsection, even before full T-tubule formation; the latter occurred concurrent with

128 nly in the cell midsection, even before full T-tubule formation; the latter occurred concurrent with

129 ains and regulates muscle transverse tubule (T-tubule) formation in flies.

130 IRAP abundance was increased in T-tubule fractions of fasting transgenic mice, when comp

131 ased muscle glycogen, and GLUT4 targeting to T-tubule fractions was increased 5.7-fold.

132 bution of the t tubules (power of the normal t-tubule frequency: UN 8.13+/-1.12x10(5), n=57 vs. C 20.

133 The average diameter of single t-tubules from six cells was estimated to 448 +/- 172 nm

134 ysis and quantification of the remodeling of T-tubules have been a challenge and remain inconsistent

135 Atrial myocytes, lacking t-tubules, have two functionally separate groups of ryan

136 In atrial myocytes, which lack t-tubules, ICa inactivation was not changed by the treat

137 aracterized modulation of ICa by Ca2+ at the t-tubules (ie, in control cells) and surface sarcolemma

138 al maturation of hiPSC-CM, including lack of T-tubules, immature excitation-contraction coupling, and

139 , isoproterenol fails to concentrate BIN1 to t-tubules, impairing P-RyR recruitment.

140 CADs also caused loss of T tubules in rat cardiac ventricular myocytes and the op

141 ll membrane invaginations called transverse (T)-tubules in determining Ca influx and action potential

142 has been used to investigate the role of the t-tubules in Ca2+ cycling during excitation-contraction

143 ulation of dystroglycan that is expressed at t-tubules in normal skeletal muscles.

144 Moreover, we found that t-tubules in rabbit have approximately twice the diamete

145 diating the normally tight regulation of the t-tubules in response to load variation are poorly under

146 lasticity with reappearance of z-grooves and T-tubules in reverse-remodeled hearts.

147 2.2 are localized at the plasma membrane and T-tubules in rodent skeletal muscle.

148 tation-contraction coupling, the role of the t-tubules in such arrhythmogenesis has not previously be

149 with adult human ventricular cardiomyocytes, T-tubules in T3+Dex-treated hiPSC-CM were less organized

150 nal membrane at the cell surface than in the T-tubules (in nM/microm(2): 1.43 vs. 1.06 during a cardi

151 An isoform of amphiphysin 2 concentrated at T-tubules induced tubular plasma membrane invaginations

152 Osmotic shock, which selectively eliminates T-tubules, induced a greater reduction in L- versus TTCC

153 We also found that T-tubule inner folds are rescued by expression of the BI

154 regularity of T-tubules to give an index of T-tubule integrity (TTint), which provides a global eval

155 red 6 d after MI for 4 wk each increased the T-tubule integrity at the remote and border zones.

156 that the action potential at the transverse (t)-tubules is longer than at the surface membrane in mam

157 We calculated that Ca influx at the T-tubules is 1.3 times that at the cell surface (4.9 vs.

158 a cardiac action potential, Ca entry at the T-tubules is 2.2 times that at the cell surface (3.0 vs.

159 nctional density of NCX and Na/K pump in the t-tubules is 3-3.5-fold higher than in the external sarc

160 e concentration of Ca2+ flux pathways in the t-tubules is important in producing a uniform increase i

161 al muscle-specific protein that localizes to T tubules, is essential for coupling membrane depolariza

162 ation of the sarcoplasmic reticulum (SR) and T-tubule junction, leading to disruption of the SR signa

163 f Ca channels is present at cell surface and T-tubule junctions ( approximately 35).

164 Due to the absence of t-tubules, L-type Ca(2+) channels were only located in t

165 e model was used to ascertain how HF-induced T-tubule loss led to altered LTCC function and early aft

166 In cardiac disease, t-tubule loss occurs and affects the systolic calcium tr

167 one, where there was also significantly more t-tubule loss, with a greater deterioration in t-tubule

168 nce, it led to approximately 25% decrease in T-tubule LTCC amplitude.

169 Rat, but not human, T-tubule LTCCs had open probability similar to crest LTC

170 eceptors was further tested by rendering the T-tubule lumen inaccessible to bath-applied ET-1.

171 However, the mechanisms controlling t-tubule maintenance and whether these factors differ be

172 AmpII is intricately involved in t-tubule maintenance.

173 and in heart failure, so that changes in the t-tubules may contribute to the functional changes obser

174 location and co-location of proteins at the t-tubules may contribute to the generation of arrhythmog

175 endent actin polymerization to stabilize the T-tubule membrane at cardiac Z discs.

176 reduction in beta1-AR density in surface and T-tubule membrane fractions without a change in beta2-AR

177 we reveal that dysferlin is enriched in the t-tubule membrane of mature skeletal muscle fibers.

178 BIN1+13+17 recruits actin to fold the T-tubule membrane, creating a 'fuzzy space' that protect

179 Z-disc protein that binds to proteins in the t-tubule membrane.

180 N1 or BIN1+13+17) creates transverse-tubule (t-tubule) membrane microfolds, which facilitate ion chan

181 are both localized at intercalated disc and T-tubule membranes in cardiomyocytes, and Na(v)1.5 coimm

182 ROS production occurs in the sarcolemmal and t-tubule membranes where NOX2 is located and sensitizes

183 and a significant fraction of ICaL reside in T-tubule membranes where they are transmurally regulated

184 that bridging integrator 1 (BIN1) organizes t-tubule microfolds and facilitates CaV1.2 delivery, we

185 -terminal domain), and depolarization of the T-tubule moiety of the triad (physiologic stimulation) i

186 Depolarization of the T-tubule moiety of the triad induced a rapid increase of

187 allows A-bands to be imaged independently of T-tubule morphology and simultaneously with Ca(2+) indic

188 eased, as occurs in acquired cardiomyopathy, T-tubule morphology is altered, and arrhythmia can resul

189 Consistent with these findings, t-tubule morphology, cytoplasmic penetration, and distan

190 ed heart failure, as well as preservation of T-tubule network integrity in both the left and right ve

191 The T-tubule network was analyzed in 3-dimension (3D) to mea

192 ther T3 or Dex alone, developed an extensive T-tubule network.

193 emma of myotubes but mostly localizes to the T-tubule network.

194 ecture extracting is necessary to remove non-T-tubule noise from the analysis.

195 Here we find that cardiac T tubules normally contain dense protective inner membra

196 associate in vivo where they localize to the T tubules of ventricular myocytes.

197 The transverse (t-) tubules of mammalian ventricular myocytes are invagi

198 a2 is preferentially expressed with beta2 in T-tubules of cardiac myocytes, forming alpha2beta2 heter

199 specific site of interest (crest, groove, or T-tubules of cardiomyocytes) and sealed to the membrane

200 liver precise quantities of compounds to the T-tubules of cardiomyocytes.

201 g activity of L-type calcium channels in the T-tubules of ventricular cardiomyocytes.

202 hat calcineurin and PKA co-localize near the T-tubules of ventricular myocytes.

203 The transverse tubules (t-tubules) of mammalian cardiac ventricular myocytes are

204 simulations showed that the delivery to the T-tubule opening is highly confined to the underlying Z-

205 Delivery to the crest, instead of the T-tubule opening, resulted in a much lower concentration

206 rlying Z-groove, and especially to the first T-tubule opening, where the concentration is approximate

207 fine neuronal dendrites, and, particularly, T-tubule openings of cardiac myocytes.

208 distributed and colocalized in the region of T-tubule openings, but not in other regions of the myocy

209 face topography including transverse-tubule (T-tubule) openings leading into a cell internal system t

210 o large pools of membrane, possibly caveoli, T-tubules or portions of the gigaseal.

211 nd MLP protein showed a further reduction in t-tubule organization and accelerated heart failure.

212 junctophilin-2 (JP-2), which is involved in T-tubule organization and formation of the T-tubule/sarc

213 yte Ca(2+) release is not only determined by t-tubule organization but also by the interplay between

214 rved that mitsugumin 29 (Mg29), an important t-tubule organizing protein in skeletal muscle, was indu

215 studies showed irregular distribution of the t tubules (power of the normal t-tubule frequency: UN 8.

216 iented T-tubules and longitudinally oriented T-tubules, power spectrum of the overall T-tubule system

217 T-tubule proliferation occurs without loss of the origin

218 Bridging integrator 1 (BIN1) is a T-tubule protein associated with calcium channel traffic

219 Our discovery of dysferlin as a t-tubule protein that stabilizes stress-induced Ca(2+) s

220 Cardiac transverse (T)-tubules provide a specialized structure for synchroni

221 of GLUT4 storage vesicles at sarcolemma and t-tubules rather than inducing movement of intact storag

222 potential propagation at the level of single T-tubules, recently observed in diseased cardiomyocytes.

223 Isoproterenol redistributes BIN1 to t-tubules, recruiting P-RyRs and improving the calcium t

224 tubule loss, with a greater deterioration in t-tubule regularity.

225 e multiple molecular pathways which underpin t-tubule regulation, Telethonin (Tcap) appears to be imp

226 that beta-AR antagonists can protect against T-tubule remodeling after MI, suggesting a novel therape

227 e hypothesized that beta-AR blockers prevent T-tubule remodeling and thereby provide therapeutic bene

228 to examine the effect of beta-AR blockers on T-tubule remodeling following LV MI.

229 brane dyes have boosted the discoveries that T-tubule remodeling is a significant factor contributing

230 We found that MI caused remarkable T-tubule remodeling near the infarction border zone and

231 T-tubule remodeling occurs early during LV failure.

232 cial effects of metoprolol and carvedilol on T-tubule remodeling.

233 The analysis of single t-tubules revealed novel morphological features.

234 the density of beta1-ARs in both surface and T-tubule sarcolemma (55+/-4%, n=7, P<0.001; and 45+/-10%

235 tment overlying the M-line and distinct from T-tubules, sarcoplasmic reticulum, Golgi, endoplasmic re

236 CICR process and identify disruption of the t-tubule-sarcoplasmic reticulum interaction as a possibl

237 of the sarcoplasmic reticulum than just the T-tubule-sarcoplasmic reticulum junction.

238 n T-tubule organization and formation of the T-tubule/sarcoplasmic reticulum junctions.

239 ause the density of T-tubules as well as non-T-tubule signals in the images influence the spectrum po

240 elease (CICR) in particular, and transverse (t)-tubule structure.

241 to provide an overview of recent studies of t-tubule structure and function in cardiac myocytes.

242 To assess its role in regulating t-tubule structure and function, we used Tcap knockout (

243 p is a critical, load-sensitive regulator of t-tubule structure and function.

244 ocytochemical analysis revealed that overall T-tubule structure and localization of ryanodine recepto

245 muscle LIM protein, MLP) partially restored t-tubule structure and preserved cardiac function as mea

246 Changes in t-tubule structure and protein expression occur during d

247 Moreover, preservation of t-tubule structure by Mg29 induction significantly incre

248 We applied the in situ imaging of T-tubule structure from Langendorff-perfused intact hear

249 Both mechanical overload and unloading alter t-tubule structure, but the mechanisms mediating the nor

250 hronically unloaded heart result in impaired t-tubule structure, with ineffective Ca(2+) release.

251 The t-tubules' structure appears to be specifically regulate

252 g loss of sarcolemmal organization, aberrant T-tubule structures, and increased sensitivity to membra

253 cells lacking organized transverse tubules (T-tubules) such as atrial myocytes (AMs).

254 a(2+)) signaling proteins in the transverse (t-) tubules suggests additional roles.

255 The transverse (t)-tubule system plays an essential role in healthy and

256 e display mild muscle fiber degeneration and T-tubule system abnormalities.

257 t for action potential propagation along the T-tubule system and excitation-contraction coupling.

258 ted in tubular and vesicular portions of the T-tubule system, respectively.

259 ii) abnormalities in the organization of the T-tubule system, with dilated and longitudinally oriente

260 erscored by the disrupted development of the T-tubule system.

261 ulating the effect of altered loading on the t-tubule system.

262 The transverse-tubule (T-tubule) system of ventricular myocytes is an important

263 ted T-tubules, power spectrum of the overall T-tubule systems, and averaged spacing of T-tubules.

264 which is used to represent the regularity of T-tubule systems.

265 om the SR has a greater effect on ICa in the t-tubules than at the surface sarcolemma.

266 functional and structural disruption of the t-tubules that is ameliorated by reducing external [Ca(2

267 ly afterdepolarisations, and how the loss of t-tubules that occurs during heart failure may alter the

268 tubular invaginations (transverse tubules or T-tubules) that function in depolarization-contraction c

269 a role in synchronizing Ca2+ release at the t-tubules; the amplitude of the Ca2+ transient and contr

270 It is possible that because of the lack of t-tubules these RyRs do not experience a sufficiently la

271 t Drosophila tracheoles invade flight muscle T-tubules through transient surface openings.

272 ng of electrical activity selectively at the t-tubules to directly examine this hypothesis.

273 also combined the density and regularity of T-tubules to give an index of T-tubule integrity (TTint)

274 basolateral trafficking, redirects FGF from T-tubules to surface, increasing tracheal surface ramifi

275 r canonical location in transversal tubules (T-tubules) to the non-native crest of the sarcolemma, wh

276 ux via Na(+)/Ca(2+)-exchange in longitudinal T-tubules triggers release from apposing ryanodine recep

277 In a myocyte lying flat on a coverslip, t-tubules typically progressed from its upper and lower

278 reen fluorescent protein bound reversibly to T-tubules upon activation.

279 en though we found no evidence for organized t-tubules using di-8-ANEPPS staining.

280 spholipase C-beta 1 were co-localized within T-tubules using standard immunofluorescence techniques,

281 1-mutated fish, smaller and irregular-shaped t-tubule vesicles, as well as highly disorganized termin

282 ls gated by conformational coupling with the t-tubule voltage-sensing dihydropyridine receptors.

283 Correspondingly, GLUT4-GFP translocation to T-tubules was abolished, while translocation to sarcolem

284 Access to T-tubules was not compromised, and insulin receptor dist

285 ulin receptor distribution in sarcolemma and T-tubules was unaffected by denervation or high-fat feed

286 n rat atrial and sheep HF atrial cells where t-tubules were absent, junctophilin 2 had sarcomeric int

287 In the sheep, atrial t-tubules were also lost in HF and AmpII levels decrease

288 T-tubules were visualized with sulforhodamine B dye.

289 &80% of TTX-sensitive INa is located in the t-tubules, where it generates &1/3 of t-tubular INa.

290 occurs at distinct structures (dyads) along t-tubules, where L-type Ca channels (LCCs) appose sarcop

291 of exterior membranes (surface membrane and T tubules), which acts as the voltage sensor of excitati

292 located in the plasma membrane and along the T-tubules, which mediates Ca(2)(+) entry into cardiomyoc

293 ion coupling is located predominantly at the t-tubules, which thus form a Ca(2+)-handling micro-envir

294 , intercalated discs and transverse tubules (t-tubules), while NHE1 is absent from t-tubules.

295 ,4,5 P(3) (PIP3) production was abolished in T-tubules, while PIP3 production at sarcolemma was incre

296 ), and loss of EHD1 results in overgrowth of T-tubules with excess vesicle accumulation in skeletal m

297 se GLUT4 translocation to the sarcolemma and t-tubules with similar kinetics and do not require AMPKa

298 ar vesicle depots to both the sarcolemma and t-tubules with similar kinetics, although translocation

299 T4-EGFP translocation to both sarcolemma and t-tubules with similar kinetics.

300 and M-band structures, and misalignments of T-tubules with Z-disks.

301 dies revealed electron dense material in the t-tubules within the muscle tissue of parkin knockdown z