Tnfaip1-flox Mouse

Tnfaip1, or tumor necrosis factor α -induced protein 1, was first identified in human umbilical vein endothelial cells and can be induced by TNFα. It plays crucial roles in multiple biological processes. It is involved in DNA replication, repair, and cell cycle regulation by binding to target proteins [4]. It also participates in pathways related to inflammation, oxidative stress, and neuronal development, making it important for understanding various physiological and pathological conditions. Zebrafish and mouse models have been used to study its functions.

In mouse models, neuronal-specific Tnfaip1 ablation attenuates postoperative cognitive dysfunction by preventing K48-linked ubiquitination of SNAP25, which promotes mitophagy and represses pyroptosis [1]. In zebrafish, CRISPR/Cas9-mediated knockout of tnfaip1 leads to developmental delays, microcephaly, and microphthalmia, with decreased expression of neuronal marker genes [2]. In N2a cells, knockdown of Tnfaip1 alleviates formaldehyde-induced neurotoxicity by preventing the inhibition of the Akt/CREB pathway [3]. In PC12 cells, down-regulation of Tnfaip1 suppresses Nrf2-mediated ferroptosis and alleviates oxygen glucose deprivation and reperfusion-induced neuronal damage [5]. In THP-1 macrophage-derived foam cells and apoE-/-mice, knockdown of Tnfaip1 inhibits lipid accumulation and attenuates atherosclerotic lesions through the LEENE/FoxO1/ABCA1 pathway [6]. In LPS-induced pneumonia mice, silencing Tnfaip1 alleviates inflammation, oxidative stress, and apoptosis via the PI3K/Akt/Nrf2 pathway [7].

In conclusion, Tnfaip1 is involved in diverse biological functions such as embryonic development, neuronal function, and regulation of inflammatory and oxidative stress responses. Studies using gene knockout models in mice and zebrafish have revealed its roles in postoperative cognitive dysfunction, early development, neurotoxicity, atherosclerosis, and pneumonia, providing insights into potential therapeutic targets for related diseases.