ARID5B, a member of the AT-rich interactive domain (ARID) protein family, has been implicated in multiple biological processes. It appears to play a role in hematopoiesis, particularly in B-cell development and function. In addition, it may be involved in chromatin-related regulatory pathways, as it has been associated with histone demethylation in some contexts [1,3].

In mouse models, overexpression of Arid5b led to a reduction in the proportion of circulating B cells, immature and mature B-cell fractions in the blood and bone marrow, and follicular B cells in the spleen. It also caused defects in B-cell activation and increased mitochondrial oxygen consumption rate in B cells [1]. Deletion of Arid5b in mice increased the proportion of large and small Pre-B cells and enhanced fatty acid uptake and oxidation in Pre-B cells, while reducing the proportion of immature B cells [4].

Overall, ARID5B is crucial for B-cell development and function, regulating fatty acid metabolism and proliferation at the Pre-B cell stage. Mouse models, especially those with Arid5b overexpression or deletion, have been instrumental in uncovering its role in B-cell-related biological processes and its association with childhood acute lymphoblastic leukemia (ALL), providing valuable insights into the disease mechanism [1,2,4].