Anp32b, also known as acidic leucine-rich nuclear phosphoprotein 32B, is involved in multiple biological processes. It can form complexes with various proteins to regulate important cellular functions. For example, it participates in pathways related to cell development, hematopoiesis, and viral replication, and is thus of great biological importance. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, have been crucial in studying its functions [1,2,3,4].

In hematopoietic cells, conditional deletion of Anp32b impairs the repopulation capacity and post-injury regeneration of hematopoietic stem cells (HSCs). Mechanistically, Anp32b forms a repressive complex with p53 to inhibit p53's transcriptional activity, and p53 deletion can rescue the functional defect in Anp32b-deficient HSCs. In chronic myelogenous leukemia (CML), Anp32b deletion enhances p53 transcriptional activity to impair leukemic stem cell (LSC) function and shows synergistic therapeutic effects with tyrosine kinase inhibitors [1].

In B-cell acute lymphoblastic leukemia (B-ALL) mouse models, conditional deletion of Anp32b in hematopoietic cells promotes leukemogenesis. Anp32b interacts with PU.1 and enhances its transcriptional activity, and overexpression of PU.1 suppresses B-ALL progression [2].

Deletion of Anp32b in constitutive C57BL/6-derived Anp32b-/-mice leads to severe defects in ocular development. Anp32b directly interacts with paired box protein 6 (PAX6) and enhances its transcriptional activity [3].

In mice, ANP32B-/-mice infected with H3N2 or H5N1 influenza A virus (IAV) have reduced virus loads, inflammatory cytokine response, and pathogenicity compared to ANP32B + / + mice [4].

In conclusion, Anp32b plays essential roles in cell development, hematopoiesis, and viral pathogenesis. The KO/CKO mouse models have significantly contributed to understanding its functions in diseases like CML, B-ALL, and ocular developmental defects, providing potential therapeutic targets for these diseases.