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The G(βγ)-sequestering peptide β-adrenergic receptor kinase (βARK)ct derived from the G-protein-coupled receptor kinase (GRK)2 carboxyl terminus has emerged as a promising target for gene-based heart failure therapy. Enhanced downstream cAMP signaling has been proposed as the underlying mechanism for increased β-adrenergic receptor (βAR) responsiveness. However, molecular targets mediating improved cardiac contractile performance by βARKct and its impact on G(βγ)-mediated signaling have yet to be fully elucidated.

circulation research

The Inotropic Peptide βARKct Improves βAR Responsiveness in Normal and Failing Cardiomyocytes Through G <sub>βγ</sub> -Mediated L-Type Calcium Current Disinhibition

The Inotropic Peptide βARKct Improves βAR Responsiveness in Normal and Failing Cardiomyocytes Through G βγ -Mediated L-Type Calcium Current Disinhibition

The Inotropic Peptide βARKct Improves βAR Responsiveness in Normal and Failing Cardiomyocytes Through G _βγ -Mediated L-Type Calcium Current Disinhibition