The AGPAT3 Knockout Jurkat Polyclonal Cells represent a genetically modified human T lymphocyte population engineered using CRISPR/Cas9 to disrupt the AGPAT3 gene. This product is supplied as a heterogeneous pool of cells carrying diverse loss-of-function mutations at the AGPAT3 locus, providing a robust in vitro model to study the collective consequences of impaired acyltransferase activity without clonal selection. The polyclonal format preserves biological variability while enabling reliable genotype-phenotype correlations in downstream functional assays.
These knockout cells are derived from the Jurkat cell line, an immortalized T lymphocyte model originally established from the peripheral blood of a patient with T cell acute lymphoblastic leukemia. Jurkat cells are widely employed to investigate T cell activation, signal transduction, and apoptosis, owing to their ability to recapitulate key aspects of antigen receptor signaling. Their leukemic origin makes them particularly relevant for studying oncogenic pathways, metabolic reprogramming, and therapeutic vulnerabilities in lymphoid malignancies.
AGPAT3 (1-acylglycerol-3-phosphate O-acyltransferase 3) catalyzes the conversion of lysophosphatidic acid (LPA) to phosphatidic acid (PA), a critical step in glycerophospholipid biosynthesis and lipid signaling. This enzyme resides at a central metabolic node, channeling substrates toward triacylglycerol and membrane phospholipid production. AGPAT3 expression is regulated by adipogenic transcription factors such as PPAR?? and C/EBP??, as well as by the lipogenic regulator SREBP1 and insulin signaling. Its product PA serves as a key lipid second messenger, influencing mTORC1 activation, Raf1 membrane recruitment, and PKC?? phosphorylation, while also serving as a precursor for diacylglycerol and downstream signaling cascades.
In Jurkat T cells, disruption of AGPAT3 is expected to attenuate PA synthesis and alter the balance of glycerolipid intermediates, potentially compromising membrane biogenesis and mTOR-dependent proliferative signals. The loss of AGPAT3 may render these cells more susceptible to metabolic stress and interfere with lipid droplet dynamics, offering a tractable system to probe how phospholipid metabolism supports leukemic T cell growth and survival. This model is especially valuable for dissecting the intersection of lipid metabolism and oncogenic signaling in a well-characterized hematological cancer background.
Researchers can apply the AGPAT3 Knockout Jurkat Polyclonal Cells to explore T cell-specific lipid metabolism, screen for compounds targeting metabolic vulnerabilities, or investigate mTOR signaling modulation under conditions of altered PA availability. Typical assays include immunoblotting for phospho-AKT (Ser473) and phospho-S6 (Ser235/236), RT-qPCR analysis of SREBP1 target genes, flow cytometric assessment of apoptosis (Annexin V/PI) and cell cycle, quantitative lipidomics for LPA and PA species, and proliferation-based drug sensitivity testing. For additional details or custom applications, please contact Ascent Research.
