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1 ional SR surface facing the surface membrane/transverse tubule.
2 cose transporters to the plasma membrane and transverse tubules.
3 lin is highly enriched in the sarcolemma and transverse tubules.
4 communication with the voltage sensor in the transverse tubules.
5 )1.6 plus beta1 and/or beta3 subunits in the transverse tubules.
6 Na(v)1.3, and Na(v)1.6 are localized in the transverse tubules.
7 ivation of multiple Ca2+ release sites along transverse-tubules.
8 s are organized within the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensurin
9 ) coupling in cat atrial myocytes which lack transverse tubules and contain both subsarcolemmal junct
12 colocalizes with L-type calcium channels in transverse tubules and is associated with L-type calcium
13 formed adjacent to Z-lines by apposition of transverse tubules and junctional sarcoplasmic reticulum
14 dic junctions (i.e., the close apposition of transverse tubules and sarcoplasmic reticulum [SR]), fac
15 sorcin localizes to the dyadic junctions of transverse tubules and sarcoplasmic reticulum and coimmu
16 ed triad organization with visibly malformed transverse tubules and sarcoplasmic reticulum, suggestin
17 number of gold particles associated with the transverse tubules and the sarcolemma by three-fold.
18 two novel systems of internal membranes, the transverse tubules and the sarcoplasmic reticulum (SR).
20 lut4 was highly enriched in membranes of the transverse tubules and the terminal cisternae of the tri
23 pose that these membranes, consisting of the transverse-tubules and sarcoplasmic reticulum, are dynam
24 ies of junctional sarcoplasmic reticulum and transverse tubules, and (4) attenuated mitochondrial abn
26 otoxin (TTX)-sensitive brain isoforms in the transverse tubules are small and are detectable only aft
27 D hearts displayed a marked reduction in the transverse tubule area (59% of sham) and the surface are
28 duces the targeting of these proteins to the transverse tubules as well as reducing overall protein l
29 d without affecting dysferlin trafficking to transverse tubules, but Dysf-DeltaC2A fails to support n
30 nsport is mediated by Glut4 localized in the transverse tubules; (c) insulin increases the apparent s
31 myocytes, from both rodents and humans, this transverse tubule coupling between LTCC and beta(2)AR wa
32 to disruption of E-C coupling, plasmalemmal transverse tubule degeneration, abnormal Ca(2+) homeosta
35 loss of SPEG phosphorylation of JPH2 led to transverse-tubule disruption, a precursor of HF developm
37 e length, mitochondrial density, networks of transverse tubules), force-frequency and force-length re
41 ial independence of electrical events in the transverse tubules from those responsible for the rapid
42 he importance of dysferlin and myoferlin for transverse tubule function and in the genesis of muscula
44 calized with beta1 and beta3 subunits in the transverse tubules, identified by immunostaining of alph
46 ole for brain sodium channel isoforms in the transverse tubules in coupling electrical excitation to
48 se that the molecular switch for the loss of transverse tubules in HF and their restoration following
50 sulin increases the apparent surface area of transverse tubules in skeletal muscle; and (d) insulin c
51 colocalized with the L-type Ca2+ channel in transverse tubules in wild-type skeletal muscle and reta
53 ng RV cardiomyocyte and nuclear hypertrophy, transverse tubule integrity, and connexin-43 localizatio
55 Localization of dysferlin variants to the transverse tubules is not sufficient to support normal C
56 ed AKAP100 localization at the region of the transverse tubule/junctional sarcoplasmic reticulum.
58 ardiac atrial cells lack a regular system of transverse tubules like that in cardiac ventricular cell
59 except C2B regulate Ca(2+) signalling; (iii) transverse tubule localization is insufficient for norma
61 ment improves contractile function, reverses transverse tubule loss, restores calcium transient ampli
62 use hearts causes JPH2 dephosphorylation and transverse-tubule loss associated with downstream Ca(2+)
63 sensing dihydropyridine receptors (DHPRs) in transverse tubule membrane and Ca(2+) release channel ry
64 l muscle dihydropyridine receptor transduces transverse tubule membrane depolarization into release o
65 d by Ca(2+) influx across the sarcolemmal or transverse tubule membrane neighboring the cluster, the
66 e that interacts in vivo with the sarcolemma/transverse tubule membrane system, whereas CaM binds wit
67 rom ventricle because atrial myocytes lack a transverse tubule membrane system: Ca(2+) release starts
68 uscle fiber restores a small fraction of the transverse tubule membrane voltage sensors from the inac
69 18c to block GLUT4-EGFP translocation to the transverse-tubule membrane but not the sarcolemma membra
70 Munc18c inhibited GLUT4 translocation to the transverse-tubule membrane without affecting translocati
72 es and intramembrane charge movements in the transverse tubule membranes (T-system) of frog fast twit
73 lization of the AHNAKs in close proximity to transverse tubule membranes and Z-band regions of cardia
81 ocalizes with CaV1.2 channels and PKA in the transverse tubules of isolated ventricular myocytes.
84 erlin is an integral membrane protein of the transverse tubules of skeletal muscle that is mutated or
85 C2 domains, C2A through C2G, concentrates in transverse tubules of skeletal muscle, where it stabiliz
86 phy 2B and Miyoshi myopathy, concentrates in transverse tubules of skeletal muscle, where it stabiliz
89 plasma membrane forms tubular invaginations (transverse tubules or T-tubules) that function in depola
90 uction in adult animals results in disrupted transverse tubule organization and calcium handling.
91 n function, which may include maintenance of transverse tubule organization and intracellular Ca(2+)
92 cement with S157A/S161A telethonin disrupted transverse tubule organization and prolonged the time to
93 ignificantly improved Ca(2+) homeostasis and transverse tubule organization with significantly attenu
94 d post-myocardial infarction, resulting from transverse tubule remodeling, leading to distorted beta(
95 distributed on the cell surface membrane and transverse tubules, resulting in a striated pattern.
96 se function, ie, Ca(2+) spikes at individual transverse tubule-sarcoplasmic reticulum (T-SR) junction
97 n initial segments, specialized sites at the transverse tubule/sarcoplasmic reticulum in cardiomyocyt
99 inositol trisphosphate (InsP(3)) receptor at transverse-tubule/sarcoplasmic reticulum sites in cardio
101 d take up Ca(2+) from the cytoplasm but only transverse tubules supported store-operated Ca(2+) entry
102 A critical cardiac membrane organelle is the transverse tubule system (called the t-tubule system) wh
105 natal skeletal muscle lacks a well developed transverse tubule system, the RyR3 reinforcement of CICR
108 2) tether the sarcoplasmic reticulum (SR) to transverse tubule (T-tubule) membranes, generating stabl
109 ldtype skeletal muscle EHD1 localizes to the transverse tubule (T-tubule), and loss of EHD1 results i
113 eases, especially in cells lacking organized transverse tubules (T-tubules) such as atrial myocytes (
114 -selective dye Di-8-ANEPPS demonstrated that transverse tubules (t-tubules) were absent in atrial cel
115 o lateral sarcolemma, intercalated discs and transverse tubules (t-tubules), while NHE1 is absent fro
119 g integrator 1 (cBIN1 or BIN1+13+17) creates transverse-tubule (t-tubule) membrane microfolds, which
120 aborate, unique surface topography including transverse-tubule (T-tubule) openings leading into a cel
122 ranched from the SSTN, indicating individual transverse tubules that form triads are continuous with,
123 brane (comprising the surface sarcolemma and transverse-tubules), the intracellular calcium store (th
125 ailure, beta2ARs were redistributed from the transverse tubules to the cell crest, which led to diffu
126 rial myocyte (AM) is characterized by sparse transverse tubule (TT) invaginations and slow intracellu
129 c reticulum (SR) cisternae and extensions of transverse-tubules (TT) that increase co-localization of
130 tubular system (T-system), which consists of transverse tubules (TTs) that align with sarcomeres and
133 r-protein kinase D1-Rem1 signaling increases transverse-tubule VLCC expression that results in increa
134 n via targeted delivery of ryanodine through transverse tubules, we achieve in-preparation isolation
135 entrate on tubular PM invaginations known as transverse tubules, we hypothesize that PM curvature pla
137 ack alpha2 protein and have no alpha2 in the transverse tubules, where its expression is normally enh
138 ignals are localized exclusively to the deep transverse tubules, whereas functional beta1ARs are dist
139 rain of as little as 5% affects the shape of transverse tubules, which has important implications for