From the Department of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
J Biol Chem. 2014 Feb 7;289(6):3288-93. doi: 10.1074/jbc.M113.518282. Epub 2013 Dec 16.
Sentrin/small ubiquitin-like modifier (SUMO)-specific protease 2 (SENP2) has broad de-SUMOylation activities in vitro, which is essential for embryonic heart development. Here, we show that myostatin, a key factor in skeletal muscle development, is markedly reduced in Senp2(-/-) mouse embryonic fibroblast cells and embryos. SENP2 regulates the transcription of myostatin mainly through de-SUMOylation of MEF2A. Silencing SENP2 can reduce myostatin expression and, therefore, promote myogenesis of skeletal muscle. These results reveal the important role of SENP2 in the regulation of myostatin expression and myogenesis.
泛素样蛋白特异性蛋白酶 2(SENP2)在体外具有广泛的去 SUMO 化活性,这对于胚胎心脏发育至关重要。在这里,我们表明肌肉生长抑制素(myostatin),一种在骨骼肌发育中起关键作用的因子,在 SENP2(-/-)小鼠胚胎成纤维细胞和胚胎中明显减少。SENP2 主要通过 MEF2A 的去 SUMO 化来调节肌肉生长抑制素的转录。沉默 SENP2 可以减少肌肉生长抑制素的表达,从而促进骨骼肌的成肌作用。这些结果揭示了 SENP2 在调节肌肉生长抑制素表达和成肌作用中的重要作用。