APOBR Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of Jurkat human T lymphocytes, designed to disrupt the gene encoding apolipoprotein B receptor (APOBR). This polyclonal pool provides a robust loss-of-function system for dissecting APOBR-dependent lipid uptake and metabolism in an immune cell context without clonal selection.
The Jurkat cell line, derived from a patient with acute T-cell leukemia, is a well-characterized T-lymphocyte model extensively used for signaling, immune response, and cancer studies. Its rapid proliferation and facile genetic manipulation make it ideal for generating knockout pools to explore lipid-associated pathways in T cells.
APOBR functions as a high-affinity receptor for apolipoprotein B-48 (APOB) on dietary chylomicrons, triggering clathrin-mediated endocytosis via the AP2 adaptor complex. Internalized lipids can be incorporated into lipid droplets or fuel fatty acid oxidation pathways. In antigen-presenting cells, APOBR facilitates loading of lipid antigens onto CD1 molecules for T-cell recognition. The receptor is transcriptionally regulated by PPARG, liver X receptor (LXR) agonists, and retinoic acid receptor (RAR) agonists, while dietary fat intake directly influences its expression. Downstream effectors include lipid droplet formation, chylomicron remnant catabolism, and activation of the PPAR signaling pathway, linking dietary lipids to cellular metabolic and immune functions.
In Jurkat T cells, the role of APOBR remains incompletely understood, but its knockout enables investigation of direct lipid uptake by lymphocytes and potential crosstalk with lipid antigen presentation pathways. The model is useful for studying how chylomicron-derived lipids influence T-cell metabolism, gene expression, and function under normal or dyslipidemic conditions, offering insights into postprandial hypertriglyceridemia and metabolic syndrome.
These ready-to-use polyclonal knockout cells support an array of experimental approaches: fluorescent chylomicron uptake assays quantify endocytic activity, oil red O staining visualizes neutral lipid accumulation, and lipidomic profiling identifies global lipid changes. Western blot and RT-qPCR confirm APOBR disruption and assess downstream metabolic gene expression, while flow cytometry monitors surface receptor or CD1 levels. RNA-seq enables transcriptome-wide analysis of metabolic reprogramming. The pool format is advantageous for screening PPARG or LXR modulators and interrogating lipid-dependent T-cell responses. For additional details or to order, please contact Ascent Research.
