Safb, known as scaffold attachment factor B, is a conserved RNA-binding protein essential for early mammalian development [2]. It is involved in multiple biological processes. SAFB binds to scaffold attachment region DNA elements and is also known for its RNA-binding and protein-protein interactions. It participates in gene regulation, DNA repair, mRNA and regulatory RNA processing, and interacts with chromatin-modifying complexes [4].

In mouse models, conditional deletion of Safb in adult hippocampus increases NFIB expression and oligodendrocyte formation, indicating that SAFB blocks oligodendrocyte production in murine adult hippocampal neural stem cells by enhancing Drosha-dependent cleavage of Nfib mRNA [1]. In acute myeloid leukemia (AML), perturbation of SAFB phenocopies HOXA9 knockout, decreasing AML cell proliferation, increasing differentiation and apoptosis in vitro, and prolonging survival in vivo. The HOXA9-SAFB chromatin complex represses genes associated with differentiation and apoptosis [3].

In conclusion, SAFB plays crucial roles in multiple biological processes such as neural stem cell fate determination and in maintaining AML. The use of gene knockout and conditional knockout mouse models has provided insights into SAFB's function in these processes and diseases, which helps in understanding the underlying mechanisms and potentially developing new therapeutic strategies for AML.