FUBP3, also known as far upstream element-binding protein 3, is a transcription factor that plays crucial roles in multiple biological processes. It is involved in various pathways, such as those related to immune responses, cell proliferation, and viral replication [1,2,4,5,6,7]. Its functions are of great biological importance as it impacts diseases like Alzheimer's disease, chronic myeloid leukaemia, neuroblastoma, and more [1,2,3]. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, would be valuable for in-depth functional studies of FUBP3.

In Alzheimer's disease, FUBP3 was found to mediate amyloid-β-induced neuronal NLRP3 expression. In aged wild-type and Alzheimer's disease mouse models, FUBP3 expression increased in cortical neurons. FUBP3 was required for endogenous NLRP3 expression and tau phosphorylation in the presence of amyloid-β, suggesting its role in the transition from amyloid-β deposition to tau phosphorylation [1].

In chronic myeloid leukaemia, microdeletions of the FUBP3 gene and its reduced expression were associated with poor prognostic markers. In K562 cells, decreased FUBP3 protein was linked to increased cell proliferation and survival via MAPK-ERK pathway activation [2].

In neuroblastoma, GATA2-AS1 bound with FUBP3 to repress its liquid-liquid phase separation and interaction with SUZ12, inhibiting the malate-aspartate shuttle and neuroblastoma progression [3].

For porcine epidemic diarrhea virus (PEDV), FUBP3 could suppress PEDV replication by degrading the viral nucleocapsid protein and inducing type-I interferon production [4].

In Japanese encephalitis virus (JEV) infection, knockdown of FUBP3 decreased JEV viral titer, while overexpression increased viral infectivity, indicating FUBP3's role in regulating JEV RNA replication [5].

Lnc-EST12 interacted with FUBP3 in mouse macrophages, suppressing anti-mycobacterial innate immunity [6].

In glioblastoma, FUBP3 was identified as a key candidate gene associated with immune surveillance and GBM development [7].

In clear cell renal cell carcinoma, FUBP1 and FUBP3 activated the expression of USP7, which promoted tumor progression by stabilizing HIF2α [8].

In conclusion, FUBP3 has diverse essential biological functions, regulating immune responses, cell proliferation, and viral replication. Studies using KO/CKO mouse models and other functional experiments have revealed its significance in multiple disease areas, including Alzheimer's disease, leukaemia, neuroblastoma, and viral-related diseases. Understanding FUBP3 provides insights into disease mechanisms and potential therapeutic targets.