Key result
Transgenic mice expressing the amino terminus of beta-ARK1 developed cardiac hypertrophy driven by an enhanced beta-adrenergic receptor system, which was reversed by beta-AR antagonist administration.
Population
Transgenic mice expressing an amino-terminal peptide of beta-ARK1 in the heart
Design
Preclinical
Authors
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Suggests beta-ARK1 N-terminus drives hypertrophy in mice; leaves open relevance to human cardiac disease.
The amino terminus of beta-ARK1 plays a critical role in normal beta-adrenergic receptor regulation in vivo, with its isolated expression driving cardiac hypertrophy.
Keys et al. (2003) studied Cardiac hypertrophy. Expression of beta-ARKnt (amino acid residues 50-145 of beta-ARK1) vs. Wild-type mice (implied) was evaluated on Cardiac hypertrophy and beta-AR density/signaling. Transgenic mice expressing the amino terminus of beta-ARK1 developed cardiac hypertrophy driven by an enhanced beta-adrenergic receptor system, which was reversed by beta-AR antagonist administration.
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