Does genetic deletion of Rnd3/RhoE result in mouse heart calcium leakage through upregulation of protein kinase A signaling?
Rnd3 is a novel factor involved in intracellular Ca(2+) homeostasis regulation in the heart. Deficiency of the protein induces ryanodine receptor type 2 dysfunction by a mechanism that attenuates Rnd3-mediated β2-adrenergic receptor ubiquitination, which leads to the activation of PKA signaling. Increased PKA signaling in turn promotes ryanodine receptor type 2 hyperphosphorylation, which contributes to arrhythmogenesis and heart failure.
This study found that 3-month outcomes from a brief image-based multiple behavior intervention for college students were partially sustained at 12-month follow-up.