Zfp384, also known as CIZ/NMP4 (Cas interacting zinc finger protein, Nuclear Matrix Protein 4), is a transcription factor. It is involved in regulating matrix-related proteins and is associated with pathways related to bone metabolism and immune response, playing an important role in biological processes such as bone formation and the body's response to influenza A virus infection [1,5]. Genetic models, like knockout (KO) mice, are valuable for studying its functions.

In KO mouse models, deficiency of CIZ/NMP4 suppresses the development of K/BxN-serum induced arthritis. It reduces the clinical score, soft-tissue swelling, and inflammatory cell invasion in joint tissue. It also suppresses the arthritis-induced increase in IL-1β expression, bone resorption, and the expression of RANKL and MMP-3 mRNA [1]. Nmp4-null mice show enhanced responses to intermittent PTH, increasing trabecular bone mass and being immune to disuse-induced bone loss [2]. Conditional deletion of Nmp4 in mesenchymal stem progenitor cells (MSPCs) enhances PTH-induced bone formation and the response to sclerostin antibody administration, while deletion in later osteoblast stages does not replicate these effects [3,4]. Nmp4-deficient mice are protected from H1N1 influenza infection, with reduced monocyte and neutrophil recruitment to the lungs and decreased expression of chemokine and pro-inflammatory cytokine genes [5].

In conclusion, Zfp384 plays a significant role in bone-related processes and the innate immune response. The study of Zfp384 KO/CKO mouse models has revealed its functions in arthritis, bone metabolism, and the response to influenza A virus infection, providing insights into the underlying mechanisms of these biological processes and disease conditions.