Activation of the ubiquitin proteasome pathway in a mouse model of inflammatory myopathy: a potential therapeutic target.

ABSTRACT:

Objective

Myositis is characterized by severe muscle weakness. We and others have previously shown that endoplasmic reticulum (ER) stress plays a role in the pathogenesis of myositis. The present study was undertaken to identify perturbed pathways and assess their contribution to muscle disease in a mouse myositis model.

Methods

Stable isotope labeling with amino acids in cell culture (SILAC) was used to identify alterations in the skeletal muscle proteome of myositic mice in vivo. Differentially altered protein levels identified in the initial comparisons were validated using a liquid chromatography tandem mass spectrometry spike-in strategy and further confirmed by immunoblotting. In addition, we evaluated the effect of a proteasome inhibitor, bortezomib, on the disease ph

SUBMITTER: Rayavarapu S 

PROVIDER: S-EPMC4080828 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature