APOE Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T lymphoblastoid line. This product offers a genetically heterogeneous pool in which APOE has been disrupted, enabling loss-of-function studies without clonal selection. The polyclonal format captures diverse editing outcomes, mimicking population-level gene inactivation. This model is suited for investigating APOE roles in lipid homeostasis and receptor-mediated endocytosis.
The Jurkat cell line originated from a 14-year-old male with acute T cell leukemia. These suspension-adapted T lymphoblast-like cells are widely used in immunology and cancer research, particularly for studying T cell signaling and leukemogenesis. Their robust culture characteristics and responsiveness to stimuli make them a reliable platform for functional assays. The Jurkat background provides a defined context for examining lipid metabolism in a malignant T cell setting.
APOE encodes a 34-kDa apolipoprotein central to lipid transport and cholesterol redistribution. It associates with lipoprotein particles and facilitates their clearance by binding to LDLR and LRP1. Transcription of APOE is regulated by LXR and PPAR??, while inflammatory signals such as TNF?? and IL-1?? can modulate its expression. APOE also interacts with the cholesterol efflux transporter ABCA1 and apolipoprotein APOA1. Thus, APOE disruption impacts a network encompassing LXR, PPAR??, LDLR, LRP1, VLDLR, and ABCA1.
In Jurkat cells, APOE knockout allows dissection of cell-intrinsic lipid handling independent of its systemic roles. Leukemia lines often exhibit altered lipid metabolism, making them relevant for probing how APOE loss affects proliferation, survival, and membrane dynamics. The polyclonal nature preserves editing variance, enabling observation of heterogeneous responses to lipid challenges or drugs. This population can be deployed in high-throughput formats to study receptor expression and lipid uptake in a malignant T cell background.
Typical applications include cholesterol metabolism studies, Alzheimer??s disease pathway modeling, and drug screening targeting APOE?Creceptor interactions. Assay readouts include RT-qPCR for APOE mRNA, western blotting for protein levels, ELISA for secreted APOE, fluorescent lipid uptake and cholesterol efflux assays, and flow cytometry for LDLR and LRP1. The model also supports analysis of NF-??B-mediated inflammatory regulation of APOE. For further information, contact Ascent Research.
