Anti-beta1-Adrenergic Receptor (extracellular)-APC Antibody

FC, LCI

Beta-1 adrenoceptor, Beta-1 adrenoreceptor, ADRB1, ADRB1R, B1AR

Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C

Lyophilized powder

Beta-1 adrenoceptor, Beta-1 adrenoreceptor, ADRB1, ADRB1R, B1AR - A Rabbit Polyclonal Antibody to β1-Adrenergic Receptor (extracellular) conjugated to the fluorescent dye Allophycocyanin (APC)

Rat, Mouse, human - 14/15 amino acid residues identical

Confirmed by amino acid analysis and mass spectrometry

1 mg/ml

2nd extracellular loop

Rat

41116161

β-Adrenergic receptors (βAR) belong to the superfamily of G-protein coupled receptors (GPCRs). βAR stimulation by the sympathetic nervous system or circulating catecholamines is involved in peripheral blood circulation, metabolic regulation, muscle contraction, and central neural activities. In the heart, acute βAR stimulation serves as the most powerful means to regulate cardiac output in response to a fight-or-flight situation.There are three βAR subtypes, β1AR, β2AR and β3AR, in cardiac myocytes1. The receptors consist of seven membrane-spanning domains, three intra- and three extracellular loops, an extracellular N-terminal domain, and an intracellular C-terminal tail2.β1AR is the predominant receptor subtype expressed in human cardiomyocytes. β1AR is also expressed in the kidney3. It has been implicated in adipogenesis and memory formation4.β1AR has been widely connected with heart disease. Both the downregulation and overstimulation of β1AR have been connected to myocyte apoptosis. In addition, chronic heart failure is characterized by abnormalities in β1AR signal transduction. It was demonstrated that heart failure is also inducible in animal models by overexpression of components of the β1AR signal transduction cascade. Transgenic mice overexpressing β1AR develop, with aging, heart failure similar to that observed in dilated cardiomyopathy in humans5.