文献类型： 外文期刊
作者： Li, Qinghe 1 ; Liu, Yuhong 1 ; Wang, Yuanyuan 2 ; Zhang, Qi 1 ; Zhang, Na 1 ; Song, Danli 1 ; Wang, Fei 3 ; Gao, Qianmei 1 ; Chen, Yuxin 2 ; Zhang, Gaomeng 1 ; Wen, Jie 1 ; Zhao, Guiping 1 ; Chen, Li 4 ; Gao, Yu 2 ;
作者机构： 1.Chinese Acad Agr Sci, Minist Agr & Rural Affairs, Key Lab Anim Poultry Genet Breeding & Reprod, State Key Lab Anim Biotech Breeding,Inst Anim Sci, Beijing, Peoples R China
2.Bengbu Med Univ, Sch Biol Sci, Anhui Prov Key Lab Translat Canc Res, Bengbu, Peoples R China
3.Northwest A&F Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod Shaanxi Prov, Yangling, Peoples R China
4.Zhejiang Acad Agr Sci, Inst Anim Sci & Vet, Hangzhou, Peoples R China
5.Xianghu Lab, Hangzhou, Peoples R China
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.
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