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In vivo inhibition of elevated myocardial beta-adrenergic receptor kinase activity in hybrid transgenic mice restores normal beta-adrenergic signaling and function.
Inhibition of protein kinase C alpha improves myocardial beta-adrenergic receptor signaling and ventricular function in a model of myocardial preservation.
GRK2-mediated inhibition of adrenergic and dopaminergic signaling in right ventricular hypertrophy: therapeutic implications in pulmonary hypertension.