SAB4502707
Anti-RYR2 antibody produced in rabbit
affinity isolated antibody
Synonym(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
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 564 kDa
species reactivity
human, mouse, rat
concentration
~1 mg/mL
technique(s)
ELISA: 1:1000
immunohistochemistry: 1:50-1:100
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... RYR2(6262)
General description
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).
Immunogen
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.
Biochem/physiol Actions
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.
Features and Benefits
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
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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Storage Class Code
10 - Combustible liquids
WGK
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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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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