C1-Ten Is a Protein Tyrosine Phosphatase of Insulin Receptor Substrate 1 (IRS-1), Regulating IRS-1 Stability and Muscle Atrophy
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- C1-Ten Is a Protein Tyrosine Phosphatase of Insulin Receptor Substrate 1 (IRS-1), Regulating IRS-1 Stability and Muscle Atrophy
- Koh, Ara; Lee, Mi Nam; Yang, Yong Ryoul; Jeong, Heeyoon; Ghim, Jaewang; Noh, Jeongeun; Kim, Jaeyoon; Ryu, Dongryeol; Park, Sehoon; Song, Parkyong; Koo, Seung-Hoi; Leslie, Nick R.; Berggren, Per-Olof; Choi, Jang Hyun; Suh, Pann-Ghill; Ryu, Sung Ho
- PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY; FOXO TRANSCRIPTION FACTORS; HUMAN SKELETAL-MUSCLE; GROWTH-FACTOR-II; SIGNAL-TRANSDUCTION; IN-VIVO; UBIQUITIN LIGASES; GENE-EXPRESSION; CELL-SURVIVAL; RESISTANCE
- Issue Date
- AMER SOC MICROBIOLOGY
- MOLECULAR AND CELLULAR BIOLOGY, v.33, no.8, pp.1608 - 1620
- Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, insulin resistance, or increased levels of glucocorticoids. This results from reduced levels of insulin receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation of FoxO transcription factors. However, the precise mechanism of reduced IRS-1 under a catabolic condition is unknown. Here, we report that C1-Ten is a novel protein tyrosine phosphatase (PTPase) of IRS-1 that acts as a mediator to reduce IRS-1 under a catabolic condition, resulting in muscle atrophy. C1-Ten preferentially dephosphorylated Y612 of IRS-1, which accelerated IRS-1 degradation. These findings suggest a novel type of IRS-1 degradation mechanism which is dependent on C1-Ten and extends our understanding of the molecular mechanism of muscle atrophy under catabolic conditions. C1-Ten expression is increased by catabolic glucocorticoid and decreased by anabolic insulin. Reflecting these hormonal regulations, the muscle C1-Ten is upregulated in atrophy but downregulated in hypertrophy. This reveals a previously unidentified role of C1-Ten as a relevant PTPase contributing to skeletal muscle atrophy.
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