作者: A. Koh , M. N. Lee , Y. R. Yang , H. Jeong , J. Ghim
DOI: 10.1128/MCB.01447-12
关键词:
摘要: Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, resistance, or increased levels of glucocorticoids. This results from reduced receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation FoxO transcription factors. However, the precise mechanism IRS-1 a condition is unknown. Here, we report that C1-Ten novel protein tyrosine phosphatase (PTPase) acts as mediator reduce condition, resulting in muscle atrophy. preferentially dephosphorylated Y612 IRS-1, which accelerated degradation. These findings suggest type degradation dependent on extends our understanding molecular conditions. expression by glucocorticoid anabolic insulin. Reflecting these hormonal regulations, upregulated but downregulated hypertrophy. reveals previously unidentified role relevant PTPase contributing skeletal