NR07
Anti-Ryanodine Receptor Mouse mAb (C3-33)
liquid, clone C3-33, Calbiochem®
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About This Item
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41
Produits recommandés
Source biologique
mouse
Niveau de qualité
Forme d'anticorps
purified antibody
Type de produit anticorps
primary antibodies
Clone
C3-33, monoclonal
Forme
liquid
Contient
≤0.1% sodium azide as preservative
Espèces réactives
fish, canine, rat, avian, amphibian, rabbit
Fabricant/nom de marque
Calbiochem®
Conditions de stockage
OK to freeze
avoid repeated freeze/thaw cycles
Isotype
IgG1
Conditions d'expédition
wet ice
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
rat ... Ryr2(689560)
Description générale
Mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with P3X 63 AG8.653 mouse myeloma cells (see application references). Supplied as protein G purified antibody. Recognizes the ~565 kDa ryanodine receptor.
Recognizes the ~565 kDa ryanodine receptor in rat brain hippocampus. A ~565 kDa doublet representing the α and β isoforms is observed in non-mammalian vertebrates.
This Anti-Ryanodine Receptor Mouse mAb (C3-33) is validated for use in Frozen Sections, Immunoblotting, Immunoprecipitation for the detection of Ryanodine Receptor.
Immunogène
Canine
canine cardiac ryanodine receptor (RYR)
Application
Frozen Sections (1 g/ml, see application references)
Immunoblotting (1 g/ml)
Immunoprecipitation (see comments)
Conditionnement
Please refer to vial label for lot-specific concentration.
Avertissement
Toxicity: Standard Handling (A)
Forme physique
In PBS.
Reconstitution
Following initial thaw, aliquot and freeze (-20°C).
Remarque sur l'analyse
Positive Control
Rat brain hippocampus
Rat brain hippocampus
Autres remarques
A ~565 kDa doublet representing the α and β isoforms is observed in non-mammalian vertebrates. In frozen sections, Clone C3-33 strongly stains the myofiber consistent with the sarcoplasmic reticulum of the RyR. This antibody has been reported to work for immunoprecipitation; the concentration is assay-dependent. Antibody should be titrated for optimal results in individual systems.
Sitsapesan, R., et al. 1995. Trends Pharmacol. Sci.16, 386.
McPherson, P.S. and Campbell, K.P. 1993. J. Biol. Chem.268, 13765.
Meszaros, L.G., et al. 1993. Nature364, 76.
Lai, F.A., et al. 1992. Biochem. J.288, 553.
Lai, F.A., et al. 1989. Nature331, 315.
McPherson, P.S. and Campbell, K.P. 1993. J. Biol. Chem.268, 13765.
Meszaros, L.G., et al. 1993. Nature364, 76.
Lai, F.A., et al. 1992. Biochem. J.288, 553.
Lai, F.A., et al. 1989. Nature331, 315.
Informations légales
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 1
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
Certificats d'analyse (COA)
Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".
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Ioannis Smyrnias et al.
Cell calcium, 47(3), 210-223 (2010-01-29)
Narrow, tubular, inward projections of the sarcolemma ('T-tubules') are an established feature of adult mammalian ventricular myocytes that enables them to generate the whole-cell Ca2+ transients and produce coordinated contraction. Loss of T-tubules can occur during ageing and under pathological
Carmen Tarifa et al.
JACC. Basic to translational science, 8(1), 1-15 (2023-02-14)
Analysis of the spatio-temporal distribution of calcium sparks showed a preferential increase in sparks near the sarcolemma in atrial myocytes from patients with atrial fibrillation (AF), linked to higher ryanodine receptor (RyR2) phosphorylation at s2808 and lower calsequestrin-2 levels. Mathematical
Verónica Jiménez-Sábado et al.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 158, 114169-114169 (2023-01-03)
Atrial fibrillation (AF) has been associated with excessive spontaneous calcium release, linked to cyclic AMP (cAMP)-dependent phosphorylation of calcium regulatory proteins. Because β-blockers are expected to attenuate cAMP-dependent signaling, we aimed to examine whether the treatment of patients with β-blockers
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