Increase in skeletal muscle amount by an attenuation of PIP3 phosphatase SKIP

在这项研究中，我们发现，骨骼肌和肾脏富含肌醇多磷酸5-磷酸酶（SKIP）负调控胰岛素样生长因子（IGF）-1信号在骨骼肌。SKIP通过负性调节PI 3-激酶信号通路抑制IGF-1介导的蛋白质合成和肥大。结合SKIP基因杂合子敲除小鼠胫骨前肌数量增加的结果，SKIP基因可能是引起骨骼肌萎缩的关键因素。因此，SKIP可能是一个有前途的目标，为干预营养不良伴随着几个严重的疾病，包括癌症恶病质。

In this study, we revealed that skeletal muscle and kidney enriched inositol polyphosphate 5-phosphatase (SKIP) negatively regulated insulin-like growth factor (IGF)-1 signal in the skeletal muscle. SKIP inhibited IGF-1 mediated protein synthesis and hypertrophy through the negative regulation of PI 3-kinase signaling pathway. Together with the results that SKIP heterozygous knockout mice exhibited increased amount of tibialis anterior skeletal muscle, SKIP is likely to be a key factor that trigger hypotrophy of skeletal muscle. Thus, SKIP may be a promising target for the intervention of hypotrophy accompanied by several severe diseases including cancer cachexia.