Phosphorylation of the ryanodine receptor 2 at serine 2030 is required for a complete β-adrenergic response.

ABSTRACT: During physical exercise or stress, the sympathetic system stimulates cardiac contractility via β-adrenergic receptor (β-AR) activation, resulting in protein kinase A (PKA)-mediated phosphorylation of the cardiac ryanodine receptor RyR2. PKA-dependent "hyperphosphorylation" of the RyR2 channel has been proposed as a major impairment that contributes to progression of heart failure. However, the sites of PKA phosphorylation and their phosphorylation status in cardiac diseases are not well defined. Among the known RyR2 phosphorylation sites, serine 2030 (S2030) remains highly controversial as a site of functional impact. We examined the contribution of RyR2-S2030 to Ca²⁺ signaling and excitation-contraction coupling (ECC) in a transgenic mouse with an ablated RyR2-S2030 phosphoryl

SUBMITTER: Potenza DM 

PROVIDER: S-EPMC6363414 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature