Ubiquitin Proteasome Dysfunction in Human Hypertrophic and Dilated Cardiomyopathies

Abstract

Proteasome activity in HCM and failing human hearts is impaired in the absence of changes in proteasome protein content or availability of proteolytic active sites. These data provide strong evidence that posttranslational modifications to the proteasome may account for defective protein degradation in human cardiomyopathies.