The AGPS Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for the disruption of the AGPS gene in the Jurkat T lymphocyte cell line. This knockout model provides researchers with a powerful loss-of-function tool to investigate ether lipid biosynthesis and its implications in peroxisomal biology and immune cell function.
Jurkat cells are an immortalized human T lymphocyte line originally derived from a patient with acute T cell leukemia. They are a widely utilized model system for studying adaptive immune responses, including T cell receptor signaling, cytokine production, and cytotoxic activity. The Jurkat background offers a physiologically relevant host to explore how peroxisomal ether lipid metabolism influences T cell biology and leukemogenesis.
AGPS encodes alkylglycerone phosphate synthase, a peroxisomal enzyme that catalyzes the exchange of the acyl group of acyl-dihydroxyacetonephosphate for a long-chain fatty alcohol, yielding alkyl-dihydroxyacetonephosphate??a critical intermediate in ether lipid biosynthesis. This reaction is transcriptionally regulated by PPAR-alpha and SREBP1 and requires PEX19 for peroxisomal targeting. AGPS functions in concert with interacting partners PEX7 and FAR1, and its product is reduced by alkylglycerone phosphate reductase to ultimately generate plasmalogens and platelet-activating factor. Consequently, AGPS operates at a central metabolic node connecting peroxisomal fatty alcohol utilization to the synthesis of membrane phospholipids and lipid mediators.
Disruption of AGPS in Jurkat T cells abolishes plasmalogen production, impairing membrane antioxidant defenses, altering lipid raft composition, and potentially affecting T cell receptor-mediated activation and apoptosis. Given the role of ether lipids in membrane fluidity and signaling platform organization, this knockout model is instrumental for dissecting AGPS-dependent pathways in immune synapse formation and cytokine signaling. Furthermore, the leukemia origin of Jurkat cells allows investigation of ether lipid dependency in malignant T cell survival and stress response.
This polyclonal knockout cell population is well-suited for a broad spectrum of functional studies, including ether lipid metabolism analysis, peroxisomal disorder modeling such as rhizomelic chondrodysplasia punctata type 3, and lipid signaling research. Researchers can employ LC-MS-based plasmalogen quantification, lipidomics profiling, fatty alcohol incorporation assays, AGPS enzymatic activity measurements, and Western blotting or RT-qPCR for gene expression validation. Downstream phenotypic assessments, including flow cytometric analysis of apoptosis, can further elucidate the role of AGPS in oxidative stress resistance and cell fate decisions. For further information on this product or related services, please contact Ascent Research.
