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首页> 外文期刊>Molecular and Cellular Biology >Regulation of Myoblast Differentiation by the Nuclear Envelope Protein NET39
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Regulation of Myoblast Differentiation by the Nuclear Envelope Protein NET39

机译：核包膜蛋白NET39调节成肌细胞分化。

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Recently, several transmembrane proteins of the nuclear envelope have been implicated in regulation of signaling and gene expression. Here we demonstrate that the nuclear lamina-associated nuclear envelope transmembrane protein NET39 (Ppapdc3) functions as a negative regulator of myoblast differentiation, in part through effects on mTOR signaling. We found that NET39 is highly expressed in cardiac and skeletal muscle tissues and becomes strongly upregulated during cultured myoblast differentiation. Knockdown of NET39 by RNA interference in myoblasts strongly promoted differentiation, whereas overexpression of NET39 repressed myogenesis. Proteomic analysis of NET39 complexes immunoprecipitated from myotubes, in combination with other methods, identified mTOR as an interaction partner of NET39. We found that ectopic expression of NET39 in myoblasts negatively regulated myogenesis by diminishing mTOR activity, which in turn decreased insulin-like growth factor II production and autocrine signaling. Our results indicate that NET39 is part of the regulatory machinery for myogenesis and raise the possibility that it may be important for muscle homeostasis.
机译：近来，核包膜的几种跨膜蛋白已涉及信号传导和基因表达的调节。在这里，我们证明核层相关的 n 核 e nvelope t 膜蛋白NET39（Ppapdc3）作为成肌细胞分化的负调节剂，部分通过对mTOR信号传导的影响。我们发现NET39在心脏和骨骼肌组织中高度表达，并在成肌细胞分化过程中强烈上调。 RNA干扰在成肌细胞中对NET39的抑制作用强烈促进分化，而NET39的过表达则抑制了肌发生。从肌管中免疫沉淀的NET39复合物的蛋白质组学分析与其他方法相结合，确定了mTOR是NET39的相互作用伴侣。我们发现，NET39在成肌细胞中的异位表达通过减少mTOR活性来负调控肌发生，从而降低了胰岛素样生长因子II的产生和自分泌信号传导。我们的结果表明，NET39是肌发生的调节机制的一部分，并提高了它对肌肉稳态的重要性。

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