The BTN1A1 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the human hepatic epithelial cell line SK-HEP-1, with targeted disruption of the BTN1A1 gene. This knockout pool preserves genetic heterogeneity, providing a physiologically relevant loss-of-function model without clonal selection bias. SK-HEP-1 cells originate from the ascites of a liver adenocarcinoma patient, carry a TP53 mutation, and display epithelial-mesenchymal plasticity, making them a robust platform for hepatocellular carcinoma research. The product enables dissection of BTN1A1’s immunomodulatory functions in a cancer context.
SK-HEP-1 is a widely used hepatic cancer model that retains key malignant features, including aberrant p53 signaling and the capacity for dynamic epithelial?Cmesenchymal transition. These properties facilitate studies of metastasis, tumor?Cimmune interactions, and drug resistance. Introducing a BTN1A1 knockout into this background creates a system to examine how loss of this butyrophilin family protein influences intercellular signaling and may expose tumor cell vulnerabilities.
BTN1A1 is a butyrophilin family member structurally related to co-inhibitory B7 molecules. Its expression is induced by IFN-?? and TNF-?? via NF-kB and STAT3. At the immune synapse, BTN1A1 interacts with the TCR/CD3 complex, SHP-2, ZAP70, and CD28. These interactions modulate proximal TCR signaling, including LCK phosphorylation, ZAP70 activation, and the LAT?CPLCG1 axis, ultimately regulating MAPK and NF-kB cascades. Downstream, BTN1A1 influences IL-2 transcription and STAT5-driven T cell proliferation, positioning it as a key node in immune checkpoint regulation.
In SK-HEP-1 cells, BTN1A1 ablation likely disrupts immune checkpoint control and cytokine secretion, offering a model to study tumor immune evasion. Given hepatocellular carcinoma??s reliance on BTN1A1-related pathways for suppressing T cell responses, the knockout cells allow investigation of altered immunogenicity and T cell engagement. Additionally, the connection between BTN1A1 and lipid metabolism permits exploration of metabolic?Cimmune crosstalk within a TP53-mutant, plastic epithelial background, enhancing its value for combined metabolic and immuno-oncology studies.
This polyclonal knockout pool supports diverse assays, including NF-kB luciferase reporter analyses, phospho-specific flow cytometry, and western blotting for MAPK and STAT5 signaling. Co-culture with T cells enables measurement of proliferation (CFSE) and cytokine secretion (IL-2, IFN-?? ELISA), while RNA-seq, RT-qPCR, and co-immunoprecipitation provide deeper mechanistic insight. Applications span immune checkpoint research, drug target validation, and functional genomics in hepatocellular carcinoma and metabolic disorders. For further technical specifications, pricing, or ordering assistance, please contact Ascent Research.
