Mitochondrial CaMKII phosphoproteome.

ABSTRACT: Mice overexpressing CaMKII in myocardial mitochondria have dilated cardiomyopathy that appears to be exclusively driven by metabolic defects that lead to reduced ATP production. Phosphoproteomics study of mitochondrial proteins supports the metabolomics data.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Eleonora Corradini  

LAB HEAD: Albert J.R. Heck

PROVIDER: PXD004631 | Pride | 2020-07-31

REPOSITORIES: Pride