Alkbh1, or alkB homolog 1, is a member of the AlkB superfamily of Fe (II) and α -ketoglutarate -dependent dioxygenases. It functions as a demethylase, reversing DNA methylation and repairing DNA damage. It is involved in various biological processes such as post-transcriptional gene expression regulation, osteogenic reprogramming, and glycolysis regulation, and is associated with diseases like cancer, chronic kidney disease-related vascular calcification, and more [1,2,3].

In mice, Alkbh1 knockout impairs chemically induced gastric carcinogenesis. Mechanistically, it mediates DNA 6mA demethylation to repress gene expression, disrupting NRF1 binding capacity and suppressing AMPK signaling, thus facilitating tumorigenesis [4]. In another study, knockdown of Alkbh1 in human mesenchymal stem cells (hMSCs) and 3T3-L1 preadipocytes inhibits adipogenic differentiation, while overexpression leads to increased adipogenesis. It regulates adipogenic differentiation via the HIF-1 signaling pathway [5].

In conclusion, Alkbh1 plays essential roles in multiple biological processes through its demethylase activity. Mouse models, including gene knockout and knockdown models, have been crucial in revealing its functions in diseases such as cancer and adipogenic differentiation, providing insights into potential therapeutic targets for these diseases.