huBCMA(TNFRSF17) Mouse

The TNFRSF17 gene, also known as BCMA, encodes a protein belonging to the tumor necrosis factor receptor superfamily. This protein is predominantly expressed in mature B lymphocytes, particularly plasma cells, with lower expression in early B cells and non-B cells ^[1-2]. As a type III transmembrane glycoprotein, TNFRSF17 plays a critical role in B cell survival and differentiation, acting as a key regulator of B cell maturation ^[2]. Functionally, TNFRSF17 primarily acts as a receptor for the B cell-activating factor (BAFF). Upon BAFF binding, it activates both the classical NF-κB pathway and the non-classical MAPK8/JNK pathway, subsequently regulating downstream gene expression to promote B cell survival, proliferation, and antibody secretion. Furthermore, TNFRSF17 can interact with TNFR-associated factors (TRAFs) 1, 2, and 3, further mediating physiological processes related to cell differentiation and growth ^[1-2]. Multiple studies have demonstrated that the TNFRSF17 gene and its protein are associated with various B cell-related diseases. Notably, this gene exhibits abnormally high expression in diseases such as multiple myeloma and systemic lupus erythematosus, rendering it a potential therapeutic target for these conditions ^[3-4].

The huBCMA(TNFRSF17) mouse is a humanized model constructed using gene editing technology, where the mouse BCMA endogenous extracellular domain was replaced with the human BCMA extracellular domain. Homozygous huBCMA(TNFRSF17) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of multiple myeloma, systemic lupus erythematosus, and various B cell-related diseases and for the development of BCMA-targeted drugs.