Reduced Ca2+ current, charge movement, and absence of Ca2+ transients in skeletal muscle deficient in dihydropyridine receptor beta 1 subunit.
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Functional analysis of a frame-shift mutant of the dihydropyridine receptor pore subunit (alpha1S) expressing two complementary protein fragmentsModulation of L-type Ca2+ current but not activation of Ca2+ release by the gamma1 subunit of the dihydropyridine receptor of skeletal muscleCa(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channelChannelopathies of skeletal muscle excitabilityA component of excitation-contraction coupling triggered in the absence of the T671-L690 and L720-Q765 regions of the II-III loop of the dihydropyridine receptor alpha(1s) pore subunit.Excitation-contraction coupling in skeletal muscle of a mouse lacking the dihydropyridine receptor subunit gamma1Altered inactivation of Ca2+ current and Ca2+ release in mouse muscle fibers deficient in the DHP receptor gamma1 subunitCa2+ sparks in embryonic mouse skeletal muscle selectively deficient in dihydropyridine receptor alpha1S or beta1a subunits.The junctional SR protein JP-45 affects the functional expression of the voltage-dependent Ca2+ channel Cav1.1Mutations of calcium channel beta subunit genes in miceStac3 has a direct role in skeletal muscle-type excitation-contraction coupling that is disrupted by a myopathy-causing mutation.Recovery of Ca2+ current, charge movements, and Ca2+ transients in myotubes deficient in dihydropyridine receptor beta 1 subunit transfected with beta 1 cDNA.The beta 1a subunit is essential for the assembly of dihydropyridine-receptor arrays in skeletal muscle.Molecular origin of the L-type Ca2+ current of skeletal muscle myotubes selectively deficient in dihydropyridine receptor beta1a subunitDifferential regulation of skeletal muscle L-type Ca2+ current and excitation-contraction coupling by the dihydropyridine receptor beta subunit.Contribution of ryanodine receptor type 3 to Ca(2+) sparks in embryonic mouse skeletal muscleInvolvement of the carboxy-terminus region of the dihydropyridine receptor beta1a subunit in excitation-contraction coupling of skeletal muscleFunctional expression of the L-type calcium channel in mice skeletal muscle during prenatal myogenesis.Truncation of the carboxyl terminus of the dihydropyridine receptor beta1a subunit promotes Ca2+ dependent excitation-contraction coupling in skeletal myotubes.Ca2+ current and charge movements in skeletal myotubes promoted by the beta-subunit of the dihydropyridine receptor in the absence of ryanodine receptor type 1.RyR1/RyR3 chimeras reveal that multiple domains of RyR1 are involved in skeletal-type E-C couplingCa2+-dependent excitation-contraction coupling triggered by the heterologous cardiac/brain DHPR beta2a-subunit in skeletal myotubesIn vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.The alpha1 subunit EGL-19, the alpha2/delta subunit UNC-36, and the beta subunit CCB-1 underlie voltage-dependent calcium currents in Caenorhabditis elegans striated muscle.Troponin T3 regulates nuclear localization of the calcium channel Cavβ1a subunit in skeletal muscle.Intramolecular ex vivo Fluorescence Resonance Energy Transfer (FRET) of Dihydropyridine Receptor (DHPR) β1a Subunit Reveals Conformational Change Induced by RYR1 in Mouse Skeletal MyotubesRem uncouples excitation-contraction coupling in adult skeletal muscle fibers.Bimolecular fluorescence complementation and targeted biotinylation provide insight into the topology of the skeletal muscle Ca ( 2+) channel β1a subunit.Evolving concepts on the age-related changes in "muscle quality".Association of calcium channel alpha1S and beta1a subunits is required for the targeting of beta1a but not of alpha1S into skeletal muscle triads.Regulation of maximal open probability is a separable function of Ca(v)beta subunit in L-type Ca2+ channel, dependent on NH2 terminus of alpha1C (Ca(v)1.2alpha).Functional impact of the ryanodine receptor on the skeletal muscle L-type Ca(2+) channelRem inhibits skeletal muscle EC coupling by reducing the number of functional L-type Ca2+ channels.Voltage-gated calcium channels and idiopathic generalized epilepsies.The skeletal L-type Ca(2+) current is a major contributor to excitation-coupled Ca(2+) entry.Increased CaVbeta1A expression with aging contributes to skeletal muscle weaknessNeuromuscular synaptic patterning requires the function of skeletal muscle dihydropyridine receptors.Voltage-controlled Ca2+ release and entry flux in isolated adult muscle fibres of the mouse.Role of the C terminus of the alpha 1C (CaV1.2) subunit in membrane targeting of cardiac L-type calcium channels.Differential effects of Ca2+ channel beta1a and beta2a subunits on complex formation with alpha1S and on current expression in tsA201 cells.
P2860
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P2860
Reduced Ca2+ current, charge movement, and absence of Ca2+ transients in skeletal muscle deficient in dihydropyridine receptor beta 1 subunit.
description
1996 nî lūn-bûn
@nan
1996 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
1996 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
name
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@ast
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@en
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@nl
type
label
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@ast
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@en
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@nl
prefLabel
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@ast
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@en
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@nl
P2093
P2860
P1433
P1476
Reduced Ca2+ current, charge m ...... idine receptor beta 1 subunit.
@en
P2093
P2860
P304
P356
10.1016/S0006-3495(96)79446-8
P407
P577
1996-11-01T00:00:00Z