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1 current amplitude or open probability of the cardiac ryanodine receptor.
2 body MA3-916, also raised against the canine cardiac ryanodine receptor.
3 es and regulation by CaM of the skeletal and cardiac ryanodine receptors.
4 alcium release activity of both skeletal and cardiac ryanodine receptors.
5 rm of verticilide (ent-verticilide) inhibits cardiac ryanodine receptor 2 (RyR2) and exhibits antiarr
7 coplasmic reticulum can be normalized by the cardiac ryanodine receptor 2 (RyR2) inhibitor, dantrolen
8 rm a protein complex that is associated with cardiac ryanodine receptor 2 (RyR2) SR Ca(2+) release ch
9 ch is caused by loss-of-function variants in cardiac ryanodine receptor 2 (RyR2), is an emerging caus
10 ired beta-agonist-induced denitrosylation of cardiac ryanodine receptor 2 (RyR2), resulting in calciu
11 hibitor of cardiac calcium release channels [cardiac ryanodine receptor 2 (RyR2)] at doses threefold
12 in the developed world, is characterized by cardiac ryanodine receptor 2 channels that are hyperphos
14 2+-binding protein that associates with both cardiac ryanodine receptors and L-type Ca2+ channels and
15 Ca(2+)-ATPase [SERCA2a], phospholamban, and cardiac ryanodine receptor), and contractile function (m
16 nteract with and disrupt the function of the cardiac ryanodine receptor Ca(2+) release channel (RyR2)
17 ith PKA-mediated hyperphosphorylation of the cardiac ryanodine receptor/Ca(2+)-release channel, which
18 arcoplasmic reticulum (SR) Ca2+ leak via the cardiac ryanodine receptor/calcium release channel (RyR2
19 ple targets in cardiac muscle, including the cardiac ryanodine receptor/calcium release channel (RyR2
21 constructed models of the pore region of the cardiac ryanodine receptor channel (RyR2) monomer and te
22 study, we addressed whether Zn(2+) modulates cardiac ryanodine receptor gating and Ca(2+) dynamics in
24 ia syndrome associated with mutations in the cardiac ryanodine receptor gene (Ryr2) in the majority o
25 prevalence of mutations in the RYR2-encoded cardiac ryanodine receptor in cases with exertional sync
26 These results appear to indicate that the cardiac ryanodine receptor is capable of being activated
28 hmias in a mouse model of CPVT by inhibiting cardiac ryanodine receptor-mediated Ca(2+) release and t
29 including voltage-gated Na and Ca channels, cardiac ryanodine receptors, Na/Ca-exchanger, and SR Ca-
30 hypothesis for elevated Ca(2+) leak through cardiac ryanodine receptors (ryanodine receptor 2 [RyR2]
32 ion to determine whether Ca(2+) can regulate cardiac ryanodine receptor (RyR) channel gating from wit
36 1.2 Ca(2+)/CaM-dependent inactivation, while cardiac ryanodine receptor (RyR2) activity remained unaf
37 connection between molecular defects in the cardiac ryanodine receptor (RyR2) and arrhythmias remain
38 with mutations in the genes encoding for the cardiac ryanodine receptor (RyR2) and cardiac calsequest
40 ic disorder associated with mutations in the cardiac ryanodine receptor (RyR2) and cardiac calsequest
41 determine the CaM binding properties of the cardiac ryanodine receptor (RyR2) and to identify potent
42 d its metabolite, doxorubicinol, bind to the cardiac ryanodine receptor (RyR2) and to the sarco/endop
46 a widely used pharmacological agonist of the cardiac ryanodine receptor (RyR2) Ca(2+) release channel
48 To study the function and regulation of the cardiac ryanodine receptor (RyR2) Ca(2+) release channel
49 CPVT) require spontaneous Ca(2+) release via cardiac ryanodine receptor (RyR2) channels affected by g
50 e crossing region (the proposed gate) of the cardiac ryanodine receptor (RyR2) completely abolishes l
55 NH2-terminal region (residues 1-543) of the cardiac ryanodine receptor (RyR2) harbors a large number
57 m the sarcoplasmic reticulum mediated by the cardiac ryanodine receptor (RyR2) is a fundamental event
61 t the single-channel level, oxidation of the cardiac ryanodine receptor (RyR2) is known to activate a
63 Ca from sarcoplasmic reticulum (SR) via the cardiac ryanodine receptor (RyR2) may contribute to cont
64 s a hetero-oligomer with FKBP12, whereas the cardiac ryanodine receptor (RyR2) more selectively assoc
67 tachycardia (CPVT) is caused by mutations in cardiac ryanodine receptor (RyR2) or calsequestrin (Casq
68 n kinase A (PKA) hyperphosphorylation of the cardiac ryanodine receptor (RyR2) resulting in dissociat
69 isease often caused by point variants in the cardiac ryanodine receptor (RyR2) that enhance diastolic
70 bility to reduce the open probability of the cardiac ryanodine receptor (RyR2) while having no effect
71 riments we characterized another site on the cardiac ryanodine receptor (RyR2) with which ryanoids in
72 rdiac death due to missense mutations in the cardiac ryanodine receptor (RyR2), an intracellular Ca2+
73 in calcium handling in myocytes, such as the cardiac ryanodine receptor (RyR2), critically regulate c
74 lation of the calcium (Ca2+) release channel/cardiac ryanodine receptor (RyR2), required for cardiac
81 sphodiesterase 4D3 (PDE4D3) was found in the cardiac ryanodine receptor (RyR2)/calcium-release-channe
82 ssible for flecainide to directly affect the cardiac ryanodine receptor (RyR2); however, an extracell
83 lasmic reticulum (SR) Ca(2+) release through cardiac ryanodine receptors (RyR2) aggravate cardiac rem
85 kinase A (PKA)-dependent phosphorylation of cardiac ryanodine receptors (RyR2) is linked to the deve
86 eins FKBP12.6 and FKBP12 are associated with cardiac ryanodine receptors (RyR2), and cAMP-dependent p
87 ses sudden cardiac death due to mutations in cardiac ryanodine receptors (RyR2), calsequestrin, or ca
88 r tachyarrhythmias (VTs) in a mouse model of cardiac ryanodine-receptor (RyR2)-linked catecholaminerg
91 nels is a critical step in the activation of cardiac ryanodine receptors (RyRs) and release of Ca2+ v
93 cytes and single channel recordings from rat cardiac ryanodine receptors (RyRs) incorporated into pla
94 ein kinase A-mediated phosphorylation of the cardiac ryanodine receptor (the Ca(2+) release channel o
95 rdia (CPVT) is a familial disorder caused by cardiac ryanodine receptor type 2 (RyR2) or calsequestri
99 tabolic labeling experiments showed that the cardiac ryanodine receptor was phosphorylated at additio