Spop deficiency impairs adipogenesis and promotes thermogenic capacity in mice

文献类型： 外文期刊

第一作者： Li, Qinghe

作者： Li, Qinghe;Liu, Yuhong;Zhang, Qi;Zhang, Na;Song, Danli;Gao, Qianmei;Zhang, Gaomeng;Wen, Jie;Zhao, Guiping;Wang, Yuanyuan;Chen, Yuxin;Gao, Yu;Wang, Fei;Chen, Li;Chen, Li

作者机构：

期刊名称：PLOS GENETICS （ 影响因子：3.7； 五年影响因子：4.5 ）

ISSN： 1553-7404

年卷期： 2024 年 20 卷 12 期

页码：

收录情况： SCI

摘要： As the adaptor protein that determines substrate specificity of the Cul3-SPOP-Rbx1 E3 ligase complex, SPOP is involved in numerous biological processes. However, its physiological connections with adipogenesis and thermogenesis remain poorly understood. In the current study, we report that the conditional knockout of Spop in mice results in substantial changes in protein expression, including the upregulation of a critical factor associated with thermogenesis, UCP1. Loss of SPOP also led to defects in body weight gain. In addition, conditional knockout mice exhibited resistance to high-fat-diet-induced obesity. Proteomics analysis found that proteins upregulated in the knockout mice are primarily enriched for functions in glycolysis/gluconeogenesis, oxidative phosphorylation, and thermogenesis. Furthermore, Spop knockout mice were more resilient during cold tolerance assay compared with the wild-type controls. Finally, the knockout of SPOP efficiently impaired adipogenesis in primary preadipocytes and the expression of associated genes. Collectively, these findings demonstrate the critical roles of SPOP in regulating adipogenesis and thermogenic capacity in mice.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序