NT5E, also known as CD73, encodes an ecto-5'-nucleotidase expressed on the cell surface of various cell types. It hydrolyzes extracellular adenosine monophosphate into adenosine and inorganic phosphate, thus performing numerous homeostatic functions in healthy organs and tissues. It is also associated with the p53 signaling pathway which regulates cell senescence [1,2].

In a mouse model of alcohol-related liver fibrosis (ALF), the absence of NT5E was protective. CD73/NT5E had a more significant regulatory effect on the activation, proliferation, and apoptosis of hepatic stellate cells (HSCs) compared with CD39/ENTPD1. Mechanistically, CD73/NT5E regulated ALF and the activation and senescence of stellate cells by binding to Aurora kinase A (AURKA) and inhibiting its ubiquitination, while downregulating p53 signaling [1].

In summary, NT5E is crucial for maintaining cellular homeostasis and is involved in important biological processes. The study of NT5E-knockout mouse models has revealed its role in alcohol-related liver fibrosis, indicating that NT5E could be a potential therapeutic target for ALF [1].

References:

1. Liu, Zhenni, Wu, Baoming, Liu, Xueqi, Xu, Tao, Lv, Xiongwen. 2023. CD73/NT5E-mediated ubiquitination of AURKA regulates alcohol-related liver fibrosis via modulating hepatic stellate cell senescence. In International journal of biological sciences, 19, 950-966. doi:10.7150/ijbs.80461. https://pubmed.ncbi.nlm.nih.gov/36778123/

2. Kordaß, Theresa, Osen, Wolfram, Eichmüller, Stefan B. 2018. Controlling the Immune Suppressor: Transcription Factors and MicroRNAs Regulating CD73/NT5E. In Frontiers in immunology, 9, 813. doi:10.3389/fimmu.2018.00813. https://pubmed.ncbi.nlm.nih.gov/29720980/