AGPAT2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human acute T cell leukemia Jurkat cell line. This product comprises a heterogeneous pool of cells carrying targeted disruptions in the AGPAT2 gene, providing a robust loss-of-function model for studying AGPAT2-dependent lipid metabolism and signaling. The polyclonal nature preserves diverse knockout alleles, making it ideally suited for experiments where averaging over multiple clones is acceptable and for screening applications where cellular heterogeneity may reveal dynamic pathway responses.
The Jurkat host cell line is an immortalized human T lymphocyte model established from a patient with acute T cell leukemia. These cells are extensively used to investigate T cell receptor signaling, activation, apoptosis, and leukemogenesis. Their rapid growth, ease of transfection, and well-characterized signaling pathways make them a versatile platform for genetic manipulation. Jurkat cells express key T cell surface markers and retain the ability to produce cytokines upon stimulation, offering a physiologically relevant background for exploring the intersection of lipid metabolism and immune function in a malignant T cell context.
AGPAT2 encodes 1-acylglycerol-3-phosphate O-acyltransferase 2, a critical acyltransferase that converts lysophosphatidic acid (LPA) to phosphatidic acid (PA) in the de novo biosynthesis of glycerophospholipids and triacylglycerols. This enzymatic step is a key branch point, with PA serving as a precursor for membrane phospholipids (via CDP-diacylglycerol) and storage lipids. AGPAT2 activity is regulated by upstream factors such as PPAR??, SREBP1, and insulin signaling, and it cooperates with other AGPAT isoforms (AGPAT1, AGPAT3, AGPAT4), GPAT enzymes, and acyl-CoA donors. Downstream, AGPAT2 influences the production of diacylglycerol, triacylglycerol, membrane phospholipids, and lipid second messengers that orchestrate signal transduction cascades.
Disruption of AGPAT2 in Jurkat T cells offers a powerful model to dissect lipid-mediated regulation of immune cell function. Given that T cell activation involves metabolic reprogramming with enhanced lipid synthesis, knockout of this enzyme impairs PA production, potentially altering membrane composition, lipid droplet formation, and signaling events dependent on lipid intermediates. This model is directly relevant to congenital generalized lipodystrophy type 1 (CGL1), caused by AGPAT2 mutations, and its associated metabolic dysfunctions including insulin resistance and metabolic syndrome. The Jurkat background further enables exploration of how altered lipid handling in T cells contributes to disease pathogenesis and aberrant immune responses.
These polyclonal knockout cells are suitable for a wide range of applications, including lipidomic profiling and metabolic flux analysis to map lipid pathway alterations, T cell activation assays to assess functional consequences, and phospholipid profiling to quantify membrane architecture changes. Researchers can employ flow cytometry, Western blotting, RT-qPCR, and lipid droplet staining to validate target disruption and downstream effects. The model supports studies of lipid signaling in immune cells, lipodystrophy disease modeling, and metabolic reprogramming in T cell activation. For additional information, please contact Ascent Research.
