Noncanonical Form of ERAD Regulates Cardiac Hypertrophy.

ABSTRACT:

Background

Cardiac hypertrophy increases demands on protein folding, which causes an accumulation of misfolded proteins in the endoplasmic reticulum (ER). These misfolded proteins can be removed by the adaptive retrotranslocation, polyubiquitylation, and a proteasome-mediated degradation process, ER-associated degradation (ERAD), which, as a biological process and rate, has not been studied in vivo. To investigate a role for ERAD in a pathophysiological model, we examined the function of the functional initiator of ERAD, valosin-containing protein-interacting membrane protein (VIMP), positing that VIMP would be adaptive in pathological cardiac hypertrophy in mice.

Methods

We developed a new method involving cardiac myocyte-specific adeno-associated virus serovar 9-mediated e

SUBMITTER: Blackwood EA 

PROVIDER: S-EPMC9797446 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature