Nmi-KO Mouse

Nmi, also known as N-Myc and STAT Interactor protein, is an interferon-inducible protein. It participates in various cellular activities, including being involved in multiple signaling pathways such as NF-κB, MAPK, JAK, TGFβ/Smad, and STAT-related pathways [1,2,5]. It plays a significant role in tumorigenesis, immune responses, and inflammation processes, making it important in understanding disease mechanisms [1,2,6]. Genetic models, like knockout mouse models, can be valuable for studying its functions.

In cancer research, Nmi shows abnormal expression in multiple tumors. In breast cancer, loss of Nmi promotes progression via epithelial-mesenchymal transition, and it inhibits cancer stem cell traits by down-regulating hTERT [1,3]. In colorectal cancer, it promotes cell proliferation through the TGFβ/Smad pathway by upregulating STAT1 [5]. In pancreatic cancer, it promotes tumor progression and gemcitabine resistance via the STAT3-IFIT3 axis [7]. In hepatocellular carcinoma, it promotes progression via BDKRB2 and the MAPK/ERK pathway [8]. In sepsis, Nmi is a DAMP molecule that promotes inflammation by binding to TLR4 on macrophages and activating the NF-κB pathway, and its expression is increased in neutrophils and monocytes of sepsis patients [2,6]. In influenza A virus infection, Nmi-knockout mice have increased survival rate, decreased weight loss, lower viral replication, and attenuated lung inflammation. Nmi facilitates ubiquitination and proteasome-dependent degradation of IRF7 through TRIM21 to limit the IAV-triggered innate immunity [4].

In conclusion, Nmi is a multifunctional protein involved in key biological processes like tumorigenesis, immune responses, and inflammation. Gene-knockout mouse models have been crucial in revealing its role in diseases such as cancer, sepsis, and viral infections. Understanding Nmi's functions provides potential molecular targets for cancer treatment, as well as insights into the mechanisms of sepsis and viral infections [1,2,4-8,10].