AMPK activation stimulates myofibrillar protein degradation and expression of atrophy-related ubiquitin ligases by increasing FOXO transcription factors in C2C12 myotubes
| Autor: | Kazuki Nakashima, Yoko Yakabe |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
medicine.medical_specialty
Ubiquitin-Protein Ligases Muscle Fibers Skeletal Muscle Proteins Protein degradation AMP-Activated Protein Kinases Protein Serine-Threonine Kinases Applied Microbiology and Biotechnology Biochemistry Analytical Chemistry Cell Line Tripartite Motif Proteins Mice Ubiquitin AMP-activated protein kinase Myofibrils Multienzyme Complexes Internal medicine medicine Animals Phosphorylation Protein kinase A Molecular Biology Transcription factor SKP Cullin F-Box Protein Ligases biology Chemistry Myogenesis Organic Chemistry Skeletal muscle AMPK Forkhead Transcription Factors General Medicine Ribonucleotides musculoskeletal system Aminoimidazole Carboxamide Enzyme Activation Muscular Atrophy medicine.anatomical_structure Endocrinology Gene Expression Regulation biology.protein Biotechnology |
| Zdroj: | Bioscience, biotechnology, and biochemistry. 71(7) |
| ISSN: | 0916-8451 |
| Popis: | In skeletal muscle, AMP-activated protein kinase (AMPK) is a metabolic master switch regulating glucose and lipid metabolism. Recently, AMPK has been implicated in the control of protein synthesis in skeletal muscle, but the effect of AMPK activation on myofibrillar protein degradation has yet to be elucidated. The present study was designed to examine the effect of 5-aminoimidazole-4-carboxamide-1-beta-D-ribonucleoside (AICAR)-induced AMPK signaling on effector mechanisms of myofibrillar protein degradation and the expression of atrophy-related genes (atrogin-1/MAFbx, MuRF1, proteasome C2 subunit, calpains, cathepsin B, and caspase-3) in C2C12 myotubes. AICAR stimulated myofibrillar protein degradation (as measured by N(tau)-methylhistidine release), while also increasing the levels of atrogin-1/MAFbx and MuRF1 mRNA, but the expression of other atrophy-related genes was not enhanced by AICAR treatment in C2C12 myotubes. AICAR also stimulated the level of FOXO transcription factors mRNA and protein in C2C12 myotubes. These results indicate that activation of AMPK stimulates myofibrillar protein degradation through the expression of atrogin-1/MAFbx and MuRF1 by increasing FOXO transcription factors in skeletal muscles. |
| Databáze: | OpenAIRE |
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