In Stock Cell Lines
The FGL1 Knockout CMT-U27 Cell Line is a CRISPR/Cas9-edited canine knockout cell line derived from the CMT-U27 mammary tumor epithelial line. It disrupts FGL1, an immune checkpoint ligand that binds LAG-3 on T cells to suppress immunity. FGL1 is regulated by IL-6, STAT3, and NF-??B, and its knockout allows study of tumor-T cell interactions without FGL1-mediated inhibition. Ideal for tumor immunology and immunotherapy research, this model supports T cell proliferation, cytokine release, and tumor-killing assays, and enables mechanistic studies of the FGL1?CLAG-3 axis involving SHP1 and SHP2 phosphatases. For more information, contact Ascent Research.
The FGL1 Knockout CMT-U27 Cell Line is a CRISPR/Cas9-edited canine knockout cell line designed for biomedical research. It features targeted disruption of the FGL1 gene, which encodes fibrinogen-like protein 1, an immune checkpoint regulator that suppresses T cell activity. Derived from the CMT-U27 canine mammary tumor epithelial cell line, this engineered model provides a stable, reproducible loss-of-function system for studying tumor-intrinsic immune evasion mechanisms. It is supplied as a ready-to-use cell line, enabling straightforward integration into existing experimental workflows.
The CMT-U27 cell line was established from a spontaneously arising canine mammary tumor, representing an epithelial cell model that replicates many hallmarks of human breast carcinoma. Canine mammary tumors develop naturally in immune-competent animals, making them valuable for translational immuno-oncology research. Their epithelial origin and tumorigenic phenotype make CMT-U27 cells particularly suited for examining how carcinomas exploit the FGL1?CLAG-3 axis to evade immune detection.
FGL1 functions as a major ligand for Lymphocyte Activation Gene 3 (LAG-3), an inhibitory receptor on activated T cells. The FGL1?CLAG-3 interaction triggers recruitment of SHP1 and SHP2 phosphatases to the T cell receptor (TCR) complex, leading to dephosphorylation of signaling intermediates and attenuation of T cell activation, proliferation, and cytokine secretion. FGL1 expression is transcriptionally upregulated by interleukin-6 (IL-6) through activation of STAT3 and NF-??B, and is further influenced by MAPK signaling cascades. This regulatory network links inflammatory and oncogenic pathways to the suppression of antitumor immunity.
In the CMT-U27 background, knockout of FGL1 enables researchers to dissect the direct contribution of tumor-cell-derived FGL1 to immune checkpoint engagement. Co-culture experiments with canine T cells allow functional assessment of how loss of FGL1 restores T cell proliferation, cytokine production (e.g., IL-2, IFN-??), and cytotoxic activity. This system facilitates interrogation of the FGL1?CLAG-3 signaling axis in a species-matched, epithelial tumor setting, helping to differentiate its role from other LAG-3 ligands such as galectin-3 and LSECtin, and to explore combination immunotherapies that co-target multiple inhibitory pathways.
Typical applications include tumor immunology, immune checkpoint regulation, cancer immunotherapy, and LAG-3 biology. The cell line is validated for use in Western blotting to confirm FGL1 knockout, flow cytometry to monitor LAG-3 surface expression on co-cultured T cells, co-immunoprecipitation to probe FGL1?CLAG-3 interaction, and ELISA-based assays to quantify secreted cytokines. Additionally, it can be employed in T cell proliferation and tumor-killing assays to measure immune function restoration. For detailed product information, lot-specific data, and custom gene editing solutions, please contact Ascent Research.
