The BTN1A1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, offering a powerful loss-of-function model to investigate the biological roles of butyrophilin subfamily 1 member A1 (BTN1A1). This product features a broad polyclonal pool of cells carrying targeted disruptions in the BTN1A1 gene, enabling robust functional studies without the selective pressures of single-cell cloning. The knockout model provides a reliable platform to dissect BTN1A1-mediated pathways in intestinal epithelial biology, lipid metabolism, and tumorigenesis.
The parental HT29 cell line is a well-established human colorectal adenocarcinoma epithelial model originally isolated from a primary tumor, extensively utilized in cancer biology, intestinal physiology, and drug absorption research. HT29 cells retain key characteristics of intestinal epithelial cells, including the ability to form polarized monolayers and differentiated phenotypes under appropriate culture conditions, making them an ideal system for studying barrier function, transport processes, and oncogenic signaling. Their widespread use in colorectal cancer studies and inflammatory bowel disease research underscores their translational relevance.
BTN1A1 encodes a transmembrane butyrophilin protein that scaffolds xanthine oxidoreductase (XOR) and perilipin 2 (PLIN2) to mediate lipid droplet secretion, critical for lipid trafficking. BTN1A1 also strengthens epithelial adhesion through interactions with integrins and cytoskeletal proteins, modulating E-cadherin and ??-catenin, key to tissue integrity. Its expression is regulated by upstream factors including prolactin, STAT5, PPAR??, and butyrate, and it interacts with T cell immunoreceptors, implicating immune-epithelial crosstalk. Downstream, BTN1A1 regulates XOR, PLIN2, lipid droplets, and adhesion complexes, positioning it at the intersection of metabolic and structural epithelial pathways.
In HT29 colorectal adenocarcinoma cells, BTN1A1 disruption impairs lipid droplet formation and secretion, altering lipid homeostasis and energy metabolism, processes frequently dysregulated in cancer. Loss of BTN1A1-mediated adhesion may compromise barrier integrity, measurable by transepithelial electrical resistance (TEER) and junctional protein localization. Its immune-regulatory roles also enable examination of epithelial-immune interactions relevant to inflammatory bowel disease and tumor surveillance. These multifaceted effects make this polyclonal knockout population a valuable tool for deciphering BTN1A1 contributions to colorectal cancer progression and intestinal pathology.
Researchers can employ the BTN1A1 Knockout HT29 Polyclonal Cells in a diverse array of assays, including Western blotting, RT-qPCR, and immunofluorescence to confirm knockout efficiency and analyze downstream pathway alterations. Functional studies such as lipid droplet staining, migration assays, and TEER measurements enable the assessment of lipid metabolism, cell motility, and barrier function, respectively. Flow cytometry can be utilized to profile surface adhesion molecules and immune-related receptors. These applications support investigations into colorectal cancer mechanisms, intestinal barrier function, lipid storage disorders, immune-epithelial interactions, and drug transport dynamics. For additional technical details, please contact Ascent Research.
