Abstract
Atrophy of skeletal muscle is a serious consequence of numerous diseases, including cancer and AIDS. Successful treatments for skeletal muscle atrophy could either block protein degradation pathways activated during atrophy or stimulate protein synthesis pathways induced during skeletal muscle hypertrophy. This perspective will focus on the signalling pathways that control skeletal muscle atrophy and hypertrophy, including the recently identified ubiquitin ligases muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx), as a basis to develop targets for pharmacologic intervention in muscle disease.
MeSH terms
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Animals
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Calcineurin / metabolism
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Humans
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Hypertrophy / metabolism
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Insulin-Like Growth Factor I / metabolism
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Ligases / metabolism
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Muscle Proteins / metabolism
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Muscle, Skeletal / metabolism*
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Muscle, Skeletal / pathology*
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Muscular Atrophy / metabolism*
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Phosphatidylinositol 3-Kinases / metabolism
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Protein Serine-Threonine Kinases*
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-akt
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Receptors, Adrenergic, beta-2 / metabolism
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SKP Cullin F-Box Protein Ligases*
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Signal Transduction / physiology*
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Tripartite Motif Proteins
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Ubiquitin-Protein Ligases*
Substances
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Muscle Proteins
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Proto-Oncogene Proteins
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Receptors, Adrenergic, beta-2
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Tripartite Motif Proteins
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Insulin-Like Growth Factor I
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FBXO32 protein, human
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SKP Cullin F-Box Protein Ligases
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TRIM63 protein, human
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Ubiquitin-Protein Ligases
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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Calcineurin
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Ligases