Loss of SPEG Inhibitory Phosphorylation of Ryanodine Receptor Type-2 Promotes Atrial Fibrillation.

ABSTRACT:

Background

Enhanced diastolic calcium (Ca²⁺) release through ryanodine receptor type-2 (RyR2) has been implicated in atrial fibrillation (AF) promotion. Diastolic sarcoplasmic reticulum Ca²⁺ leak is caused by increased RyR2 phosphorylation by PKA (protein kinase A) or CaMKII (Ca²⁺/calmodulin-dependent kinase-II) phosphorylation, or less dephosphorylation by protein phosphatases. However, considerable controversy remains regarding the molecular mechanisms underlying altered RyR2 function in AF. We thus aimed to determine the role of SPEG (striated muscle preferentially expressed protein kinase), a novel regulator of RyR2 phosphorylation, in AF pathogenesis.

Methods

Western blotting was performed with right atrial biopsies from patients with pa

SUBMITTER: Campbell HM 

PROVIDER: S-EPMC7508800 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature