The HAVCR1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the T-47D breast ductal carcinoma line. This loss-of-function model targets the HAVCR1 gene, encoding the phosphatidylserine receptor TIM-1. The polyclonal format provides a heterogeneous pool of edited cells, suitable for population-level assays without clonal selection, enabling investigation of HAVCR1-dependent processes in a cancer-relevant epithelial context.
The T-47D host cell line is a widely employed model of hormone-responsive breast cancer, characterized by robust estrogen receptor (ER) and progesterone receptor (PR) expression. Derived from the pleural effusion of a patient with infiltrating ductal carcinoma, these cells retain luminal A subtype features, including hormone-dependent proliferation, intact p53, and epithelial differentiation markers. Their genetic stability and favorable culture properties make them an ideal platform for CRISPR/Cas9-mediated genome editing, allowing reproducible generation of polyclonal knockout populations for subsequent functional analyses.
HAVCR1 (TIM-1) functions as a phosphatidylserine and Hepatitis A virus receptor. Upon ligand binding by TIM-4 or exposed phosphatidylserine, it activates PI3K/AKT and NF-kB signaling, regulating T-cell proliferation, survival, and cytokine secretion. Expression is transcriptionally upregulated by IL-4, IL-13, and GATA3, leading to enhanced production of Th2 cytokines such as IL-4, IL-5, and IL-13. HAVCR1 also intersects with the MAPK pathway and modulates T-cell tolerance and apoptosis, linking it to immune homeostasis and allergic inflammation.
By ablating HAVCR1 in T-47D cells, researchers can investigate TIM-1-dependent signaling within an epithelial tumor context, complementing traditional T-cell studies. This system is particularly valuable for examining how phosphatidylserine recognition and downstream AKT/NF-kB pathways contribute to cancer cell survival, proliferation, or immune evasion. Additionally, the ER/PR-positive background permits exploration of hormonal crosstalk with TIM-1 signaling, potentially revealing novel therapeutic vulnerabilities. The knockout model thus bridges gaps between cancer biology and immunology, offering insights into the tumor microenvironment.
Typical applications include T-cell immunology assays where T-47D cells are co-cultured with lymphocytes to assess TIM-1-mediated interactions, Hepatitis A viral entry experiments, and Th2-driven disease models for asthma and allergic rhinitis. In cancer immunology, these cells support screens for TIM-1 modulators and drug target validation. Representative techniques encompass flow cytometry for surface HAVCR1, western blotting and RT-qPCR for knockout confirmation, ELISA for IL-4 and IL-5 secretion, co-immunoprecipitation with TIM-4, and phospho-AKT signaling analysis. For additional information, please contact Ascent Research.
