Abstract
Protein kinases are recognised as integral regulators of phosphorylation within beta-adrenergic receptor (β-AR) signalling pathways in the heart. In contrast, the role of protein phosphatases and dephosphorylation in β-AR pathways is less well defined. In vitro evidence suggests that protein phosphatase 2A (PP2A) regulatory subunit B55α may modulate gene transcription as a key downstream effector of β-AR signalling in cardiomyocytes. The goal of this study was to determine how loss of PP2A-B55α impacts β-AR signalling in cardiomyocytes.
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