Western blot analysis of extracts from mouse stomach and human heart using β1-Adrenergic Receptor Antibody.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing full-length human β1-Adrenergic Receptor (β1AR; +) or full-length human β2-Adrenergic Receptor (β2AR; +), using β1-Adrenergic Receptor Antibody (upper) or β2-Adrenergic Receptor (D6H2) Rabbit mAb #8513 (lower).
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Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
β1-Adrenergic Receptor Antibody recognizes endogenous levels of total human β1-Adrenergic Receptor protein. This antibody does not cross-react with β2-Adrenergic Receptor.
Human, Mouse, Rat
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly406 of human β1-Adrenergic Receptor protein. Antibodies are purified by protein A and peptide affinity chromatography.
β1-Adrenergic Receptor (β1AR) is a G protein-coupled receptor (GPCR) involved in the regulation of cardiovascular functions (1). Together with β2AR, β1AR is a major βAR in the heart. β1AR is activated by catecholamines and couples to Gαs protein, activating adenylate cyclase and increasing intracellular cAMP levels (2). Beta-blockers (βAR antagonists), one of the major class of therapeutics in cardiovascular medicine, act mostly by preventing catecholamine binding to β1AR (3).
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