The BTN1A1 Knockout 143B Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population from the 143B human osteosarcoma cell line, with disruption of the BTN1A1 gene. This polyclonal product maintains the inherent genetic diversity of the edited pool, avoiding clonal bias and enabling robust functional studies that reflect tumor heterogeneity. The loss-of-function model is optimized for investigating BTN1A1??s role in immune modulation within a bone cancer context.
The 143B cell line is a widely used human osteosarcoma model, originally derived from a primary osteosarcoma and characterized by high tumorigenicity and metastatic potential. This aggressive cell line is ideal for dissecting mechanisms of cancer progression and immune evasion, providing a clinically relevant host for studying gene knockouts that may influence the tumor-immune interface.
BTN1A1 is a type I transmembrane protein featuring extracellular immunoglobulin domains, belonging to the immunoglobulin superfamily. It acts as an immunomodulatory checkpoint molecule by engaging receptors on T cells to modulate TCR signaling. This regulation involves downstream effectors like ZAP70 and the adaptor protein LAT, and is influenced by interactions with other butyrophilins such as BTN2A2 and BTN3A1. BTN1A1 expression is transcriptionally controlled by IFN-?? and STAT factors, and its signaling alters T cell activation markers and cytokine secretion, thereby shaping the immune microenvironment.
In osteosarcoma, BTN1A1 likely facilitates immune evasion by suppressing T cell-mediated antitumor immunity. Its knockout in 143B cells is expected to relieve this inhibition, restoring T cell effector functions such as proliferation and cytokine release. This model thus offers a powerful tool to examine butyrophilin-dependent immune checkpoint pathways in bone malignancies and to screen for compounds targeting the BTN1A1?CT cell receptor axis.
Researchers can use these cells in co-culture assays with primary T cells to evaluate T cell proliferation, cytokine production via ELISA, and activation marker expression by flow cytometry. Molecular analyses including Western blot, RT-qPCR, and phospho-signaling studies can further elucidate the TCR?CZAP70?CLAT signaling cascade. Moreover, migration and invasion assays enable assessment of how BTN1A1 loss affects metastatic behavior. The model also extends to lactation biology and autoimmune disease research. For technical inquiries or custom knockout requests, please contact Ascent Research.
