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抗Human RYR2 抗体:
抗Rat (Rattus) RYR2 抗体:
抗Mouse (Murine) RYR2 抗体:
Two regions of the ryanodine receptor (显示 RYR3 抗体) calcium channel are involved in Ca(2 (显示 CA2 抗体)+)-dependent inactivation
[REVIEW] The efficacy of divalent calcium ion (Ca2 (显示 CA2 抗体)+) release in the myocardium depends on the amount of Ca2 (显示 CA2 抗体)+ loaded into the Ca2 (显示 CA2 抗体)+ store and the way in which this Ca2 (显示 CA2 抗体)* load influences the activity of the ryanodine receptor (显示 RYR3 抗体) Ca2+ release channel (RyR2).
There were substantial transmural gradients in Cav1.2 (显示 CACNA1C 抗体), KChIP2 (显示 KCNIP2 抗体), ERG (显示 KCNH2 抗体), KvLQT1 (显示 KCNQ1 抗体), Kir2.1 (显示 KCNJ2 抗体), NCX1 (显示 SLC8A1 抗体), SERCA2a (显示 ATP2A2 抗体) and RyR2 at the mRNA and, in some cases, protein level-in every case the mRNA or protein was more abundant in the epicardium than the endocardium.
phosphorylation and K201 acted similarly to change the conformation of RyR1/2 and regulate FKBP12/12.6 binding.
Common variants rs790899 and rs1891246 of RYR2 were significantly associated with HG and weight loss.
The left atrium / right atrium expression ratio was significantly increased in Atrial fibrillation for ryanodine receptor 2 - gene related to calcium uptake and release, and located on the sarcoplasmic reticulum membrane.
a direct interaction exists between RyR2 and CSQ2, is reported.
In a national cohort of RyR2 mutation-positive CPVT patients, SCD (显示 SCD 抗体), ASCD and syncope were presenting events in the majority of probands and also occurred in 36% of relatives identified through family screening.
We identified a variant in the RYR2 gene (NM_001035) which involved a change of a glycine to an arginine in position155 of the gene product (c.463G > A, p.Gly155Arg, p.G155R). This RYR2 gene mutation is a novel rare genetic variant as it was not present in any of the international databases consulted.
Data suggest that post-translational modifications (phosphorylation, oxidation, and nitrosylation) of RyR2 (ryanodine receptor 2) occur downstream of production of amyloid beta-peptides through ADRB2 (beta2-adrenergic receptor (显示 ADRB2 抗体)) Ca2 (显示 CA2 抗体)+ signaling cascade that activates PKA (protein kinase A).
The unique properties of the CaM-F142L mutation may provide novel clues on how to suppress excessive RyR2 Ca(2 (显示 CA2 抗体)+) release by manipulating the CaM-RyR2 interaction.
Cardiac adrenergic response and progression towards HF proceed unaltered in mice harboring the RyR2-S2808A mutation. Preventing RyR2-S2808 phosphorylation does not preclude a normal sympathetic response nor mitigates the pathophysiological consequences of MI.
These results also suggest that altered cytosolic Ca(2 (显示 CA2 抗体)+) activation of RyR2 represents a common defect of RyR2 mutations associated with catecholaminergic polymorphic ventricular tachycardia and atrial fibrillation, which could potentially be suppressed by carvedilol or (R)-carvedilol.
CaM and S100A1 can concurrently bind to and functionally modulate RyR1 and RyR2, but this does not involve direct competition at the RyR CaM binding site.
K4750Q mutation causes three RyR2 defects: hypersensitization to activation by cytosolic Ca2 (显示 CA2 抗体)+, loss of cytosolic Ca2 (显示 CA2 抗体)+/Mg2 (显示 MCOLN1 抗体)+-mediated inactivation, and hypersensitization to luminal Ca2 (显示 CA2 抗体)+ activation.
InsP3 dependent sarcoplasmic reticulum-Ca2 (显示 CA2 抗体)+ flux constitute the main mechanism of functional crosstalk between InsP3R2 (显示 ITPR2 抗体) and RyR2 resulting in more Ca2 (显示 CA2 抗体)+ sensitized RyRs to trigger subsequent Ca2 (显示 CA2 抗体)+-induced Ca2 (显示 CA2 抗体)+ release activation.
The heart contraction is controlled by the Ca2 (显示 CA2 抗体)+-induced Ca2 (显示 CA2 抗体)+ release between L-type Ca2 (显示 CA2 抗体)+ channels and ryanodine receptors. RyRs became more sensitive to Ca2 (显示 CA2 抗体)+ triggers without FKBP12.6 (显示 FKBP1B 抗体), leading to ventricular arrthymias.
Allele-specific silencing of RYR2 prevents life-threatening arrhythmias in genetic carriers.
Redox modification of RyR2 synergistically with CaMKII (显示 CAMK2G 抗体) phosphorylation modulates reperfusion arrhythmias.
These results demonstrate that Ryr2 controls mitochondrial Ca(2 (显示 CA2 抗体)+) dynamics and plays a specific, critical role in promoting glucose oxidation in cardiomyocytes. These findings indicate that partial RYR2 loss is sufficient to cause metabolic abnormalities seen in heart disease.
data suggest that interactions between the cytoplasmic region of S6 and the U motif of RyR2 are important for stabilizing the closed state of the channel. Mutations in the S6/U motif domain interface likely destabilize the closed state of RyR2
these results suggest that neuronal RyR2 Ca(2 (显示 CA2 抗体)+) leak due to Calstabin2 (显示 FKBP1B 抗体) deletion contributes to learning deficiency and memory impairment.
Nav1.5 (显示 SCN5A 抗体) is downregulated and INa (显示 INA 抗体) is reduced in RyR2-P2328S ventricles.
The minimal KEKE motif of TRN (显示 TNPO1 抗体) involved in the interactions with CSQ2, HRC (显示 HRC 抗体) and RyR2 within the Ca2 (显示 CA2 抗体)+ release units of cardiac sarcoplasmic reticulum has been defined.
This gene encodes a ryanodine receptor found in cardiac muscle sarcoplasmic reticulum. The encoded protein is one of the components of a calcium channel, composed of a tetramer of the ryanodine receptor proteins and a tetramer of FK506 binding protein 1B proteins, that supplies calcium to cardiac muscle. Mutations in this gene are associated with stress-induced polymorphic ventricular tachycardia and arrhythmogenic right ventricular dysplasia.
cardiac muscle ryanodine receptor
, ryanodine receptor 2 (cardiac)
, ryanodine receptor 2-like
, Ca2+ release channel
, cardiac muscle ryanodine receptor-calcium release channel
, cardiac muscle-type ryanodine receptor
, ryanodine receptor 2
, type 2 ryanodine receptor
, cardiac ryanodine receptor 2
, cardiac-type ryanodine receptor
, islet-type ryanodine receptor
, kidney-type ryanodine receptor
, ryanodine receptor type II
, calcium release channel
, ryanodine receptor type 2