{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rayavarapu S"],"funding":["NICHD NIH HHS","NCRR NIH HHS","NIAMS NIH HHS","NIH HHS"],"pagination":["3248-58"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4080828"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["65(12)"],"pubmed_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"],"journal":["Arthritis and rheumatism"],"pubmed_title":["Activation of the ubiquitin proteasome pathway in a mouse model of inflammatory myopathy: a potential therapeutic target."],"pmcid":["PMC4080828"],"funding_grant_id":["K26-OD-011171","5U54-HD-053177","UL1-RR-031988","R24 HD050846","2R24-HD-050846-06","P30 HD040677","P30-HD-40677","5P30-HD-040677-10","R01 AR050478","R01-AR-050478","K26 OD011171","UL1 RR031988","U54 HD053177"],"pubmed_authors":["Kinder TB","Tappeta K","Brown KJ","Hathout Y","Coley W","Rayavarapu S","Cakir E","Nagaraju K","Van der Meulen JH","Dillingham BC"],"additional_accession":[]},"is_claimable":false,"name":"Activation of the ubiquitin proteasome pathway in a mouse model of inflammatory myopathy: a potential therapeutic target.","description":"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","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Dec","modification":"2025-04-19T08:54:45.74Z","creation":"2019-03-27T01:31:21Z"},"accession":"S-EPMC4080828","cross_references":{"pubmed":["24022788"],"doi":["10.1002/art.38180"]}}