Molecular Changes in Sub-lesional Muscle Following Acute Phase of Spinal Cord Injury.
Charleston, United States. In Neurochem Res, Sep 2015
Western blot analyses performed on the visibly red, central portion of the gastrocnemius muscle showed significantly higher expression of muscle specific E3 ubiquitin ligases (muscle ring finger-1 and muscle atrophy f-box) and significantly lower expression of phosphorylated Akt-1/2/3 in the injury group compared to the sham group.
[Mechanism, diagnosis, and treatment of steroid myopathy].
Tokyo, Japan. In Brain Nerve, 2013
Recent studies have shown that steroid-mediated induction of ubiquitin ligases (atrogin-1, muscle RING finger-1) and suppression of mammalian/mechanistic target of rapamycin cause an imbalance between anabolism and catabolism of muscle proteins, resulting in muscle atrophy.
Molecular regulation of skeletal muscle mass.
Australia. In Clin Exp Pharmacol Physiol, 2010
The present review focuses on the role and regulation of pathways involving Akt, atrogin-1 and muscle ring finger-1 (MuRF1; atrogenes), peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and striated activator of Rho signalling (STARS), with exercise and disease.
Cardiac muscle ring finger-1--friend or foe?
Chapel Hill, United States. In Trends Cardiovasc Med, 2010
The ubiquitin ligase muscle ring finger-1 (MuRF1) binds creatine kinase, leading to its ubiquitination and possible degradation.
The ubiquitin-proteasome system in spongiform degenerative disorders.
Atlanta, United States. In Biochim Biophys Acta, 2008
The link between aberrant ubiquitination and spongiform neurodegeneration has been strengthened by the discovery that a null mutation in the E3 ubiquitin-protein ligase mahogunin ring finger-1 (Mgrn1) causes an autosomal recessively inherited form of spongiform neurodegeneration in animals.
Angiotensin II as candidate of cardiac cachexia.
New Orleans, United States. In Curr Opin Clin Nutr Metab Care, 2006
RECENT FINDINGS: In animals, angiotensin II produces weight loss through a pressor-independent mechanism, accompanied by decreased levels of circulating and skeletal muscle insulin-like growth factor-1 and increased mRNA levels of the ubiquitin ligases atrogin-1 and Muscle RING finger-1 in skeletal muscle.