SAB4502707
Anti-RYR2 antibody produced in rabbit
affinity isolated antibody
Synonyme(s) :
RYR-2, cardiac muscle ryanodine receptor-calcium release channel, cardiac muscle-type ryanodine receptor, ryanodine receptor 2
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About This Item
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41
Produits recommandés
Source biologique
rabbit
Conjugué
unconjugated
Forme d'anticorps
affinity isolated antibody
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
buffered aqueous solution
Poids mol.
antigen 564 kDa
Espèces réactives
human, mouse, rat
Concentration
~1 mg/mL
Technique(s)
ELISA: 1:1000
immunohistochemistry: 1:50-1:100
Numéro d'accès NCBI
Numéro d'accès UniProt
Conditions d'expédition
wet ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... RYR2(6262)
Description générale
Anti-RYR2 Antibody detects endogenous levels of total RYR2 protein.
RYR2 (ryanodine receptor 2) is an intracellular Ca2+ release channel present on the sarcoplasmic reticulum (SR). It forms tetramer with four types 2 RyR polypeptides (RyR2) and four FK506 binding proteins (FKBP12.6).
Immunogène
The antiserum was produced against synthesized peptide derived from human RyR2.
Immunogen Range: 2774-2823
Immunogen Range: 2774-2823
Application
Anti-RYR2 antibody produced in rabbit is suitable for immunohistochemistry and indirect ELISA.
Actions biochimiques/physiologiques
RYR2 (ryanodine receptor 2) provides guidance to the release and transport of Ca2+ from sarcoplasmic reticulum (SR) to the cytoplasm during cardiac muscle excitation-contraction (EC) coupling. Protein kinase A (PKA) phosphorylated RYR2 separates (FKBP12.6) to regulate the channel open probability (Po). During the process, a small portion of Ca2+ enter into the cell through the L-type Ca2+ channel, which further activates the RyR2 channel upon membrane depolarization. The activated RyR2 channel releases a large amount of Ca2+ from the SR and subsequent muscle contraction. Missense mutations in this gene cause Kazakh idiopathic ventricular tachycardia and arrhythmogenic right ventricular dysplasia.
Caractéristiques et avantages
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Forme physique
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Clause de non-responsabilité
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Code de la classe de stockage
10 - Combustible liquids
Classe de danger pour l'eau (WGK)
nwg
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Certificats d'analyse (COA)
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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.
N Tiso et al.
Human molecular genetics, 10(3), 189-194 (2001-02-13)
Arrhythmogenic right ventricular dysplasia type 2 (ARVD2, OMIM 600996) is an autosomal dominant cardiomyopathy, characterized by partial degeneration of the myocardium of the right ventricle, electrical instability and sudden death. The disease locus was mapped to chromosome 1q42--q43. We report
C Martin et al.
Neuroscience, 85(1), 205-216 (1998-06-02)
Cellular Ca2+ signalling is an important factor in the control of neuronal metabolism and electrical activity. Although the roles of Ca2+-release channels are well established for skeletal and cardiac muscle, less is known about their expression and roles in the
Dawei Jiang et al.
Proceedings of the National Academy of Sciences of the United States of America, 101(35), 13062-13067 (2004-08-24)
The cardiac ryanodine receptor (RyR2) governs the release of Ca2+ from the sarcoplasmic reticulum, which initiates muscle contraction. Mutations in RyR2 have been linked to ventricular tachycardia (VT) and sudden death, but the precise molecular mechanism is unclear. It is
K Otsu et al.
Genomics, 17(2), 507-509 (1993-08-01)
Fluorescence in situ hybridization (FISH) experiments were performed using genomic and complementary DNA probes in order to determine the location on human chromosomes for five genes expressed in cardiac and skeletal muscle sarcoplasmic reticulum. The chromosome location of each gene
S G Priori et al.
Circulation, 103(2), 196-200 (2001-02-24)
Catecholaminergic polymorphic ventricular tachycardia is a genetic arrhythmogenic disorder characterized by stress-induced, bidirectional ventricular tachycardia that may degenerate into cardiac arrest and cause sudden death. The electrocardiographic pattern of this ventricular tachycardia closely resembles the arrhythmias associated with calcium overload
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