Small Ubiquitin-like Modifier (SUMO) Protein-specific Protease 1 De-SUMOylates Sharp-1 Protein and Controls Adipocyte Differentiation

Small Ubiquitin-like Modifier (SUMO) Protein-specific Protease 1 De-SUMOylates Sharp-1 Protein and Controls Adipocyte Differentiation
复制标题

小泛素样修饰剂 (SUMO) 蛋白特异性蛋白酶 1 去 SUMO 化 Sharp-1 蛋白并控制脂肪细胞分化

DOI:
10.1074/jbc.m114.571950
复制
发表时间:
2014-08-08
影响因子:
4.8
通讯作者:
Cheng, Jinke
Cheng, Jinke
中科院分区:
生物学2区
文献类型:
--
作者:
Liu, Bingting;Wang, Tianshi;Cheng, Jinke

文献摘要

被引文献

相似文献

脂肪细胞的分化受转录级联反应的调控,主要包括CCAAT/增强子结合蛋白家族成员和核受体PPARγ。在这里,我们展示了脂肪细胞分化的缺陷以及在成脂刺激诱导的SENP1(-/-)小鼠胚胎成纤维细胞中PPARγ的表达。我们进一步确定SENP1是夏普-1的特异性去糖化蛋白水解酶,夏普-1是PPARγ转录和脂肪形成的抑制因子。SENP1通过去糖基化Sharp-1促进脂肪生成,从而释放Sharp-1对PPARγ表达和脂肪细胞分化的抑制。这些结果表明SENP1是一种新的脂肪形成调节因子。
Adipocyte differentiation is regulated by a transcriptional cascade that mainly includes CCAAT/enhancer-binding protein family members and the nuclear receptor peroxisome proliferator- activated receptor gamma (PPAR gamma). Here we show the defects in adipocyte differentiation as well as PPAR gamma expression in Senp1(-/-) mouse embryonic fibroblast cells induced by adipogenic stimuli. We further determine that SENP1 is a specific de-SUMOylation protease for Sharp-1, a repressor for PPAR gamma transcription and adipogenesis. SENP1 enhances adipogenesis through de-SUMOylation of Sharp-1, which then releases Sharp-1 repression of PPAR gamma expression and adipocyte differentiation. These results reveal SENP1 as a novel regulator in adipogenesis.