Atrogin-1, MuRF-1, and sarcopenia
نویسندگان
چکیده
منابع مشابه
Atrogin-1, MuRF-1, and sarcopenia.
Sarcopenia is one of the leading causes of disability in the elderly. Despite the growing prevalence of sarcopenia, the molecular mechanisms that control aging-related changes in muscle mass are not fully understood. The ubiquitin proteasome system is one of the major pathways that regulate muscle protein degradation, and this system plays a central role in controlling muscle size. Atrogin-1 an...
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Skeletal Muscle Atrophy and the E3 Ubiquitin Ligases, MuRF1 and 1 MAFbx/Atrogin-1 2 3 Sue C. Bodine and 1,2,3 and Leslie M. Baehr 2 4 5 Departments of Neurobiology, Physiology, and Behavior 1 ; 6 and Physiology and Membrane Biology 2 7 University of California, Davis, Davis, CA, 95616. 8 Northern California VA Health Systems 3 9 10 Running Head: E3 Ubiquitin Ligases and Sparing of Muscle Mass 1...
متن کاملSkeletal Muscle 11beta-HSD1 Controls Glucocorticoid-Induced Proteolysis and Expression of E3 Ubiquitin Ligases Atrogin-1 and MuRF-1
Recent studies demonstrated expression and activity of the intracellular cortisone-cortisol shuttle 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in skeletal muscle and inhibition of 11beta-HSD1 in muscle cells improved insulin sensitivity. Glucocorticoids induce muscle atrophy via increased expression of the E3 ubiquitin ligases Atrogin-1 (Muscle Atrophy F-box (MAFbx)) and MuRF-1 (M...
متن کاملTestosterone represses ubiquitin ligases atrogin-1 and Murf-1 expression in an androgen-sensitive rat skeletal muscle in vivo.
Skeletal muscle atrophy induced by denervation and metabolic diseases has been associated with increased ubiquitin ligase expression. In the present study, we evaluate the influence of androgens on muscle ubiquitin ligases atrogin-1/MAFbx/FBXO32 and Murf-1/Trim63 expression and its correlation with maintenance of muscle mass by using the testosterone-dependent fast-twitch levator ani muscle (LA...
متن کاملAtrophy-related ubiquitin ligases atrogin-1 and MuRF-1 are associated with uterine smooth muscle involution in the postpartum period.
The regulation of cell size depends on a delicate balance between protein synthesis and breakdown. Skeletal and cardiac muscle adapt to hormonal and neuronal stimuli and can rapidly hypertrophy and atrophy; however, the extent to which these processes occur in smooth muscle is less clear. Atrophy in striated muscle results from enhanced protein breakdown and is associated with a common transcri...
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ژورنال
عنوان ژورنال: Endocrine
سال: 2012
ISSN: 1355-008X,1559-0100
DOI: 10.1007/s12020-012-9751-7