APOC2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the APOC2 gene in human Jurkat T-lymphoblast cells. This heterogeneous pool, generated via CRISPR/Cas9, exhibits loss of apoC-II protein. The polyclonal format avoids clonal selection bias, providing a population-level tool for APOC2 loss-of-function studies. It is ideal for functional genomics and drug discovery.
Jurkat is a well-characterized, suspension-adapted T-lymphoblast cell line derived from a patient with acute lymphoblastic leukemia. It is widely employed as a model for T-cell receptor signaling, activation, proliferation, and apoptosis. Its rapid growth, ease of transfection, and infinite proliferative capacity make Jurkat an excellent host for gene-editing studies. The introduction of an APOC2 knockout into this lineage extends its utility into lipid metabolism research, offering a novel platform to investigate the intersection of immune cell biology and lipid handling pathways.
Apolipoprotein C-II serves as a critical cofactor for lipoprotein lipase (LPL), the enzyme responsible for hydrolysis of triglycerides in circulating chylomicrons and very low-density lipoproteins (VLDL). This activation releases free fatty acids for peripheral tissue uptake and reduces plasma triglyceride levels. APOC2 expression is transcriptionally regulated by nuclear receptors PPAR?? and LXR, as well as HNF4??, and is modulated by insulin and glucose. At the protein level, apoC-II directly interacts with LPL, apolipoprotein E, apolipoprotein B, and GPIHBP1 to facilitate lipoprotein docking and triglyceride processing. Downstream consequences of this interaction include generation of free fatty acids and decreased circulating triglyceride-rich particles.
Although Jurkat cells are not a traditional hepatocyte or adipocyte model, they provide a unique context for probing APOC2 function independent of liver-specific regulatory circuits. Jurkat cells express components of the lipid uptake machinery and are responsive to external lipid stimuli, enabling the study of T-cell lipid metabolism. This APOC2 knockout population allows dissection of the LPL/apoC-II axis in a lymphoid environment and serves as a null background for reconstitution with wild-type or mutant APOC2 variants. Additionally, it supports the exploration of non-canonical roles of apoC-II in immune cell signaling and lipid raft organization.
Key applications include high-throughput screening for LPL modulators, enzymatic triglyceride hydrolysis assays, western blot confirmation, RT-qPCR profiling of lipid metabolic genes, flow cytometric lipid uptake measurement, and lipid droplet staining. The polyclonal nature enhances reproducibility. For technical specifications, please contact Ascent Research.
