The BTN1A1 Knockout 786-O Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population with targeted disruption of the BTN1A1 gene. Derived from the 786-O renal epithelial adenocarcinoma cell line, this heterogeneous knockout model eliminates the need for single-cell clonal isolation while maintaining gene inactivation across the cell pool. BTN1A1 encodes an immune checkpoint protein that negatively regulates T cell activation, making this product suitable for tumor immunology and signaling studies.
The 786-O cell line, established from a primary clear cell renal carcinoma, models ccRCC and harbors VHL mutations with constitutive HIF1A activation. It is extensively used to investigate tumor microenvironment interactions, immune evasion, and hypoxia-driven signaling. These epithelial cells recapitulate key features of renal cancer, providing a disease-relevant context for studying BTN1A1 function in a tumor-intrinsic setting.
BTN1A1 inhibits T cell receptor (TCR) signaling by recruiting SHP-1 (PTPN6) and SHP-2 (PTPN11) phosphatases to its ITIM domain. This recruitment dephosphorylates LCK, ZAP70, and LAT, impairing PLCG1 activation and NFAT-dependent transcription of IL-2 and interferon-gamma. BTN1A1 is induced by IFNG through STAT1 and IRF1, and it crosstalks with PI3K/AKT and MAPK/ERK pathways, modulating cell survival and proliferation. It interacts with BTN2A1 and other butyrophilins.
In 786-O ccRCC cells, BTN1A1 ablation may alleviate intrinsic immunosuppression, potentially enhancing T cell activation in co-cultures. Loss of BTN1A1 could also modify AKT and ERK signaling cascades, altering tumor cell proliferation and survival under normoxic or hypoxic conditions. This model allows dissection of BTN1A1??s dual roles in immune checkpoint control and cell-autonomous growth regulation within the renal cancer microenvironment.
Key applications include co-culture assays to measure T cell activation (CD69, CD25) and cytokine secretion (IL-2, IFN-??) via flow cytometry and ELISA. The cells enable screening of butyrophilin-targeted checkpoint inhibitors and functional genomics studies using RNA-seq and phospho-protein analysis (p-AKT, p-ERK1/2). Standard cell-based assays for proliferation (CCK-8) and apoptosis (Annexin V) are also supported. For further details, please contact Ascent Research.
