Rad-GTPase contributes to heart rate via L-type calcium channel regulation.

ABSTRACT: Sinoatrial node cardiomyocytes (SANcm) possess automatic, rhythmic electrical activity. SAN rate is influenced by autonomic nervous system input, including sympathetic nerve increases of heart rate (HR) via activation of β-adrenergic receptor signaling cascade (β-AR). L-type calcium channel (LTCC) activity contributes to membrane depolarization and is a central target of β-AR signaling. Recent studies revealed that the small G-protein Rad plays a central role in β-adrenergic receptor directed modulation of LTCC. These studies have identified a conserved mechanism in which β-AR stimulation results in PKA-dependent Rad phosphorylation: depletion of Rad from the LTCC complex, which is proposed to relieve the constitutive inhibition of Ca_V1.2 imposed by Rad association. Here, using

SUBMITTER: Levitan BM 

PROVIDER: S-EPMC8068610 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature