Reactivation of Fetal Splicing Programs in Diabetic Hearts Is Mediated by Protein Kinase C Signaling.

The article presents a study that examines whether protein kinase C (PKC) activation in diabetic hearts induces alternative splicing abnormalities. The study reveals that phosphorylation of RNA-binding protein CELF1 by PKC is required for the regulation of splicing events altered in diabetes. It further discusses methodologies and materials used in the study such as immunohistochemistry, western blotting, and RNA sequencing.