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1 ional SR surface facing the surface membrane/transverse tubule.
2 lin is highly enriched in the sarcolemma and transverse tubules.
3 communication with the voltage sensor in the transverse tubules.
4 )1.6 plus beta1 and/or beta3 subunits in the transverse tubules.
5 Na(v)1.3, and Na(v)1.6 are localized in the transverse tubules.
6 cose transporters to the plasma membrane and 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 sorcin localizes to the dyadic junctions of transverse tubules and sarcoplasmic reticulum and coimmu
14 number of gold particles associated with the transverse tubules and the sarcolemma by three-fold.
15 two novel systems of internal membranes, the transverse tubules and the sarcoplasmic reticulum (SR).
17 lut4 was highly enriched in membranes of the transverse tubules and the terminal cisternae of the tri
19 pose that these membranes, consisting of the transverse-tubules and sarcoplasmic reticulum, are dynam
20 ies of junctional sarcoplasmic reticulum and transverse tubules, and (4) attenuated mitochondrial abn
22 otoxin (TTX)-sensitive brain isoforms in the transverse tubules are small and are detectable only aft
23 D hearts displayed a marked reduction in the transverse tubule area (59% of sham) and the surface are
24 duces the targeting of these proteins to the transverse tubules as well as reducing overall protein l
25 nsport is mediated by Glut4 localized in the transverse tubules; (c) insulin increases the apparent s
28 loss of SPEG phosphorylation of JPH2 led to transverse-tubule disruption, a precursor of HF developm
32 ial independence of electrical events in the transverse tubules from those responsible for the rapid
33 he importance of dysferlin and myoferlin for transverse tubule function and in the genesis of muscula
35 calized with beta1 and beta3 subunits in the transverse tubules, identified by immunostaining of alph
37 ole for brain sodium channel isoforms in the transverse tubules in coupling electrical excitation to
39 sulin increases the apparent surface area of transverse tubules in skeletal muscle; and (d) insulin c
40 colocalized with the L-type Ca2+ channel in transverse tubules in wild-type skeletal muscle and reta
43 ed AKAP100 localization at the region of the transverse tubule/junctional sarcoplasmic reticulum.
45 ardiac atrial cells lack a regular system of transverse tubules like that in cardiac ventricular cell
47 use hearts causes JPH2 dephosphorylation and transverse-tubule loss associated with downstream Ca(2+)
48 sensing dihydropyridine receptors (DHPRs) in transverse tubule membrane and Ca(2+) release channel ry
49 l muscle dihydropyridine receptor transduces transverse tubule membrane depolarization into release o
50 d by Ca(2+) influx across the sarcolemmal or transverse tubule membrane neighboring the cluster, the
51 e that interacts in vivo with the sarcolemma/transverse tubule membrane system, whereas CaM binds wit
52 rom ventricle because atrial myocytes lack a transverse tubule membrane system: Ca(2+) release starts
53 uscle fiber restores a small fraction of the transverse tubule membrane voltage sensors from the inac
54 18c to block GLUT4-EGFP translocation to the transverse-tubule membrane but not the sarcolemma membra
55 Munc18c inhibited GLUT4 translocation to the transverse-tubule membrane without affecting translocati
57 es and intramembrane charge movements in the transverse tubule membranes (T-system) of frog fast twit
58 lization of the AHNAKs in close proximity to transverse tubule membranes and Z-band regions of cardia
64 ocalizes with CaV1.2 channels and PKA in the transverse tubules of isolated ventricular myocytes.
67 phy 2B and Miyoshi myopathy, concentrates in transverse tubules of skeletal muscle, where it stabiliz
69 plasma membrane forms tubular invaginations (transverse tubules or T-tubules) that function in depola
70 uction in adult animals results in disrupted transverse tubule organization and calcium handling.
71 n function, which may include maintenance of transverse tubule organization and intracellular Ca(2+)
72 cement with S157A/S161A telethonin disrupted transverse tubule organization and prolonged the time to
73 distributed on the cell surface membrane and transverse tubules, resulting in a striated pattern.
74 se function, ie, Ca(2+) spikes at individual transverse tubule-sarcoplasmic reticulum (T-SR) junction
75 n initial segments, specialized sites at the transverse tubule/sarcoplasmic reticulum in cardiomyocyt
77 inositol trisphosphate (InsP(3)) receptor at transverse-tubule/sarcoplasmic reticulum sites in cardio
79 d take up Ca(2+) from the cytoplasm but only transverse tubules supported store-operated Ca(2+) entry
82 natal skeletal muscle lacks a well developed transverse tubule system, the RyR3 reinforcement of CICR
85 ldtype skeletal muscle EHD1 localizes to the transverse tubule (T-tubule), and loss of EHD1 results i
88 eases, especially in cells lacking organized transverse tubules (T-tubules) such as atrial myocytes (
89 -selective dye Di-8-ANEPPS demonstrated that transverse tubules (t-tubules) were absent in atrial cel
90 o lateral sarcolemma, intercalated discs and transverse tubules (t-tubules), while NHE1 is absent fro
94 g integrator 1 (cBIN1 or BIN1+13+17) creates transverse-tubule (t-tubule) membrane microfolds, which
95 aborate, unique surface topography including transverse-tubule (T-tubule) openings leading into a cel
97 ranched from the SSTN, indicating individual transverse tubules that form triads are continuous with,
98 brane (comprising the surface sarcolemma and transverse-tubules), the intracellular calcium store (th
99 ailure, beta2ARs were redistributed from the transverse tubules to the cell crest, which led to diffu
100 rial myocyte (AM) is characterized by sparse transverse tubule (TT) invaginations and slow intracellu
104 r-protein kinase D1-Rem1 signaling increases transverse-tubule VLCC expression that results in increa
106 ack alpha2 protein and have no alpha2 in the transverse tubules, where its expression is normally enh
107 ignals are localized exclusively to the deep transverse tubules, whereas functional beta1ARs are dist
108 rain of as little as 5% affects the shape of transverse tubules, which has important implications for
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