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

4 iomyocyte size, and development of extensive T tubules.

5 h most exhibiting an abnormal orientation of T tubules.

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

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

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

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

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

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

12 0% reduction in the contacts between jSR and T-tubules.

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

14 ecting delayed disappearance of insulin from t-tubules.

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

16 intracellular compartments to sarcolemma and t-tubules.

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

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

19 f atrial cells that were observed to contain t-tubules.

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

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

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

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

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

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

26 3D reconstructions of the t-tubules also suggested that some of them progressed fr

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

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

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

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

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

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

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

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

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

36 Paired imaging of t-tubules and Ca(2+) showed that the disorganized arrang

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

38 rt failure, which is associated with loss of T-tubules and disruption of cardiac dyads.

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

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

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

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

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

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

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

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

47 ved to be laid down in advance of developing t-tubules and similarly 'orphaned' in HF, although RyR d

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

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

50 ophilin) 2 enables close association between T-tubules and the junctional sarcoplasmic reticulum to e

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

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

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

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

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

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

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

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

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

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

61 Cardiomyocyte T tubules are important for regulating ion flux.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 te the selective localization of JPH1 at the T-tubule compartment of triads.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 and distribution at the lateral membrane and T-tubules, depending on site-specific interacting protei

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

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

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

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

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

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

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

105 lon recruitment, associated with transverse (t)-tubule disruption.

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

107 2+) release synchrony has been attributed to t-tubule disruption, but it is unknown if other factors

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 l membrane, the lateral membrane groove, and T-tubules in cardiomyocytes from wild-type (N=3), dystro

137 lar structural parallels; disorganization of t-tubules in failing cells was strikingly reminiscent of

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

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

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

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

142 2.2 are localized at the plasma membrane and T-tubules in rodent skeletal muscle.

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

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

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

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

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

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

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

150 ease synchrony, increased CaT) and preserved t-tubule integrity.

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

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

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

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

155 nsible for LTCCs recruitment to and from the T-tubules is not well known.

156 LTCCs and contributes to LTCC recruitment to T-tubules is unknown.

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

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

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

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

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

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

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

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

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

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

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

168 AmpII is intricately involved in t-tubule maintenance.

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

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

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

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

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

174 inal transmembrane domain (TMD) and bind the T-tubule membrane through their cytosolic N-terminal reg

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

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

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

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

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

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

181 plasmic reticulum (SR) to transverse tubule (T-tubule) membranes, generating stable membrane contact

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

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

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

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

186 At the lateral membrane and T-tubules, Na(v)1.5 localization and function remain ins

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

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

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

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

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

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

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

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

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

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

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

198 ional beta(3)-ARs are mostly confined to the T-tubules of healthy rat cardiomyocytes.

199 d at the groove of DeltaSIV and increased in T-tubules of mdx cardiomyocytes.

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

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

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

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

204 n microscopy, we observed that Z-grooves and t-tubule openings at the cell surface appeared gradually

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

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

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

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

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

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

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

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

213 T-tubule proliferation occurs without loss of the origin

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

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

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

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

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

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

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

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

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

223 in the joining region (mut(PG1)JPH2) caused T-tubule remodeling and dyad loss, showing that an inter

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

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

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

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

228 T-tubule remodeling occurs early during LV failure.

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

230 V) 1.2 channel abundance along cardiomyocyte T-tubules, resulting in the appearance of channel 'super

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

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

233 s exhibit a clustered distribution along the T-tubule sarcolemma of ventricular myocytes where nanome

234 Ca(V) 1.2 channel clusters decorate T-tubule sarcolemmas of ventricular myocytes.

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

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

239 We moreover assessed T-tubules sodium current by recording whole-cell sodium

240 A T-tubules sodium current could, however, not be demonstr

241 raction between LTCC and JPH2 is crucial for T-tubule stabilization.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 s because of the absence of a well-developed t-tubule system in most of these cells.

259 ted tubular systems in vitro, reminiscent of t-tubule system in muscle cells.

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

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

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

271 conditions, LTCCs are redistributed from the T-tubules to disrupt CICR.

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

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

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

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

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

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

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

279 1-mutated fish, smaller and irregular-shaped t-tubule vesicles, as well as highly disorganized termin

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

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

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

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

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

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

286 T-tubules were visualized with sulforhodamine B dye.

287 &80% of TTX-sensitive INa is located in the t-tubules, where it generates &1/3 of t-tubular INa.

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

289 nizes as distinct clusters in the groove and T-tubules which density, distribution, and organization

290 derscored by correlative imaging of RyRs and t-tubules, which enabled quantification of dyadic and no

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

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

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

294 ,4,5 P(3) (PIP3) production was abolished in T-tubules, while PIP3 production at sarcolemma was incre

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

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

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

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

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

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