GP73 regulates Hepatic Steatosis by enhancing SCAP-SREBPs interaction.
Xiaoli YangFeixiang WuJiankang ChenCui WangYongjie ZhuFeng LiQinfang HaoCuijuan DuanLi WangXueping MaDeyong ZouLi LuoYiwen ZhaoYuan CaoYuan CaoPingping ZhangPengyu ZhouShengli MaZhifeng YanJia LiYanhong ZhangCongwen WeiHui ZhongPublished in: Scientific reports (2017)
Elevated Golgi phosphoprotein 2 (GP73, also known as GOLPH2 or GOLM1) expression in serum and liver, which can be induced by viral infection and cytokine treatments, is intimately connected with liver disease, including acute hepatitis, cirrhosis and hepatocellular carcinoma (HCC). However, its pathogenic roles in hepatic diseases have never been clarified in detail. Here, we showed that the upregulated GP73 is indispensable for SREBPs activation and lipogenesis. Notably, GP73 overexpression enhanced SCAP-SREBPs binding and its Golgi trafficking even under cholesterol sufficiency. Consistent with these functional findings, GP73 blockage could alleviate tunicamycin-induced liver steatosis by reducing SREBPs activation. A significant positive correlation of GP73 with genes in lipid metabolism pathway was also identified in liver cancer based on data from The Cancer Genome Atlas (TCGA) dataset. Our findings revealed previously unrecognized role of GP73 in lipid metabolism.
Keyphrases
- single cell
- genome wide
- poor prognosis
- type diabetes
- liver failure
- cell proliferation
- gene expression
- squamous cell carcinoma
- insulin resistance
- high fat diet
- drug induced
- binding protein
- metabolic syndrome
- young adults
- fatty acid
- endoplasmic reticulum
- deep learning
- machine learning
- adipose tissue
- long non coding rna
- mechanical ventilation