Litaf-KO Mouse

Litaf, also known as lipopolysaccharide-induced tumor necrosis factor-α factor or p53-induced gene 7 (PIG7), is a transcription factor and endolysosomal protein. It activates the transcription of TNF-α, regulates the inflammatory response, and is involved in multiple cellular processes. It is associated with pathways such as the NF-κB inflammatory pathway, ubiquitination-related pathways, and the ASK1-JNK/p38 signaling pathway, playing a significant role in maintaining cellular homeostasis and in disease-related processes [1-3, 5, 7-8]. Genetic models, like gene knockout mice, are valuable tools for studying its functions.

In LITAF knockout mice, the area of atherosclerotic plaques was substantially lower compared to the control group, suggesting that LITAF promotes atherosclerotic plaque formation through the NF-κB pathway [2]. LITAF knockout mice also demonstrated exacerbated cardiac hypertrophy and fibrosis compared with wild-type mice, indicating that LITAF negatively regulates cardiac remodeling by disrupting ASK1 dimerization and blocking its activation [1].

In conclusion, Litaf is crucial in various biological processes, including membrane repair, regulation of cardiac remodeling, and modulation of cancer-related phenotypes. Studies using knockout mouse models have revealed its roles in atherosclerosis and pathological cardiac hypertrophy, providing insights into the underlying molecular mechanisms and potential therapeutic targets for these diseases.

References:

1. Xiang, Mei, Yang, Feiyan, Zhou, Yi, Wang, Pi-Xiao, Chen, Manhua. 2021. LITAF acts as a novel regulator for pathological cardiac hypertrophy. In Journal of molecular and cellular cardiology, 156, 82-94. doi:10.1016/j.yjmcc.2021.03.012. https://pubmed.ncbi.nlm.nih.gov/33823186/

2. Li, Wei-Juan, Zhou, Wen-Ping, Li, Xu-Yong, Huang, Ling, Zhang, Hui. 2023. LITAF Promotes Atherosclerotic Plaque Formation by Stimulating the NF-κB Inflammatory Pathway. In Current medical science, 43, 1201-1205. doi:10.1007/s11596-023-2802-x. https://pubmed.ncbi.nlm.nih.gov/37848750/