Anp32a, also known as acidic leucine-rich nuclear phosphoprotein-32A, is an essential host protein involved in multiple biological processes. It plays a role in histone acetylation, is a co-factor for influenza virus polymerase, and is associated with pathways like Wnt signaling. Genetic models such as gene knockout (KO) or conditional knockout (CKO) mouse models are valuable for studying its functions, which are crucial for understanding normal biological processes and disease mechanisms [4,1,2].

In Anp32a -deficient mouse models, Wnt signaling was hyper-activated in articular cartilage and the heart. Mechanistically, ANP32A inhibits target gene expression via histone acetylation masking. In the joint, this led to more severe osteoarthritis (OA), and in the heart, it potentially caused cardiac hypertrophy [2]. In zebrafish, over-expression of Anp32a mRNA promoted spinal cord regeneration and swimming capability after spinal cord injury (SCI), while its knockdown had the opposite effect, suggesting a positive role in neuronal regeneration [3].

In conclusion, Anp32a has diverse essential functions, including in histone modification, Wnt signaling regulation, and neuronal regeneration. The use of Anp32a KO mouse models has been instrumental in revealing its role in diseases such as osteoarthritis and cardiac disease, highlighting its importance in understanding these disease mechanisms.