The ABHD5 Knockout Jurkat Polyclonal Cells comprise a heterogeneous pool of Jurkat T-lymphocytes engineered with CRISPR/Cas9-mediated disruption of the ABHD5 gene. These polyclonal knockout cells offer a reliable loss-of-function model for investigating lipid metabolism in an immune context without clonal artifacts.
The Jurkat cell line is an immortalized human T-lymphocyte model derived from a 14-year-old male with acute T-cell leukemia. Widely used in immunological research, Jurkat cells provide a well-characterized system for studying T-cell signaling, activation, and metabolic reprogramming.
ABHD5 is a lipid droplet-associated co-activator of adipose triglyceride lipase (ATGL/PNPLA2), the rate-limiting enzyme in triglyceride hydrolysis. By binding perilipin 1 (PLIN1), ABHD5 activates ATGL, driving the release of diacylglycerol and free fatty acids. This lipolytic process is regulated by upstream signals such as protein kinase A (PKA), ??-adrenergic stimulation, and insulin, and it modulates downstream pathways including PPAR signaling. ABHD5 directly interacts with PNPLA2, PLIN1, and PLIN2, and operates within a network comprising PNPLA3, hormone-sensitive lipase (LIPE), and monoglyceride lipase (MGLL). CRISPR/Cas9-mediated ABHD5 disruption abrogates ATGL activation, thereby eliminating basal lipolysis and leading to lipid droplet accumulation.
In Jurkat T-cells, lipid droplets are dynamically metabolized during activation to fuel mitochondrial ??-oxidation and meet energetic demands. ABHD5-mediated lipolysis provides a critical source of free fatty acids for this process; consequently, its knockout impairs lipid droplet turnover and alters cellular energy homeostasis. These metabolic disruptions may compromise T-cell activation, proliferation, and effector functions. The ABHD5 knockout Jurkat model thus offers a valuable tool for examining the intersection of lipid metabolism and immune cell biology, and for investigating pathologies such as Chanarin-Dorfman syndrome, a neutral lipid storage disease marked by ichthyosis and multi-tissue lipid accumulation.
These polyclonal knockout cells are well-suited for investigating lipolysis in T-cell metabolism, lipid droplet dynamics, and neutral lipid storage disorders, as well as for screening ATGL pathway modulators. Compatible assays include glycerol release lipolysis assays, BODIPY lipid droplet staining, triglyceride quantification, Western blotting for ATGL and PLIN1, flow cytometry for T-cell activation markers, and Seahorse metabolic flux analysis. For further inquiries, please contact Ascent Research.
