Anti-beta1-Adrenoceptor (ext.)-ATTO Fluor-488

Antibodies

ATTO-488. Maximum absorption 501 nm; maximum fluorescence 523 nm. The fluorescence is excited most efficiently in the 480 - 515 nm range. This label is analogous to the dye fluorescein isothiocyanate (FITC) and can be used with filters used to detect FITC.

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 Conjugated to the Fluorescent Dye ATTO-488

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 control key physiological functions through signals encoded by catecholamine hormones and neurotransmitters to activate intracellular signaling pathways. These receptors belong to the amine receptor cluster of rhodopsin-like family of G-protein coupled receptors (GPCRs).The β1 adrenergic receptor (β1AR) is comprised of an extracellular N-terminus, seven membrane spanning loops (TM1-7) and an intracellular C-terminus1.β1AR couples to the stimulatory G protein Gs and thereby activates adenylyl cyclase. β1AR also couples to the inhibitory G protein Gi and can induce G protein independent signaling. Differential activation of these pathways can be modulated by different ligands2.β1AR is widely expressed in cardiac myocytes and is regulated by the microRNA (miRNA) let-7e. Following acute myocardial infraction (AMI) in rats, expression of β1AR is significantly up-regulated while the expression of miRNA let-7a (as well as miRNAs c, d, e and i) is notably down-regulated 6 and 24 hours post myocardial infarction. Blocking the up-regulation of β1AR can serve as a novel therapeutic approach for the treatment of AMI-induced arrhythmia3.β1AR is also implicated in the pathophysiology of Alzheimer's disease (AD). Administration of a partial β1AR agonist, behavioral deficits in a mouse model of AD are restored and amyloid beta and tau levels decrease as measured by regional immunohistochemistry4.