The ACOT8 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line. This heterogeneous pool harbors targeted disruptions in the ACOT8 gene, offering a loss-of-function model for studying ACOT8-dependent processes. The polyclonal format captures diverse editing events without clonal selection, providing a robust platform for functional genomics in a physiologically relevant immune cell context. These cells are suitable for a range of downstream applications, including pathway analysis and drug screening.
Jurkat cells, originating from an acute T cell leukemia patient, serve as a well-established model for T cell signaling, apoptosis, and cytokine production. These cells are highly proliferative, genetically tractable, and possess functional peroxisomes and lipid metabolic pathways. Their use in knockout studies allows the investigation of gene function within T cell biology, including the interplay between peroxisomal metabolism and immune cell activation. This makes them an ideal host for dissecting ACOT8??s role in fatty acid oxidation and lipid homeostasis.
ACOT8 encodes a peroxisomal acyl-CoA thioesterase that hydrolyzes medium- to long-chain acyl-CoAs to free fatty acids and CoA, thereby regulating fatty acid oxidation and lipid metabolism. Its expression is controlled by PPARA and PPARG and is responsive to fasting and fatty acid levels. Downstream, ACOT8 activity influences PPARA target gene networks and the availability of CoA. ACOT8 interacts with PEX5 for peroxisomal import and cooperates with beta-oxidation enzymes ACOX1, HSD17B4, EHHADH, and ACAA1. By modulating the acyl-CoA pool, ACOT8 serves as a regulatory nexus in peroxisomal lipid handling.
In Jurkat T cells, ACOT8 knockout disrupts peroxisomal beta-oxidation, perturbing the balance of free fatty acids and CoA. This alteration is expected to impact T cell lipid remodeling, energy metabolism, and redox status, processes critical for activation and effector function. The model is valuable for studying metabolic disorders, peroxisomal dysfunction, and obesity, where aberrant lipid metabolism contributes to disease pathogenesis. It enables dissection of how peroxisomal pathways intersect with immune cell signaling, providing insights into metabolic-immunological crosstalk.
This polyclonal product supports diverse applications: lipid metabolism studies, peroxisomal function assays, metabolic disease modeling, and drug target validation. Researchers can perform ACOT8-confirmation via Western blot or RT-qPCR, measure fatty acid oxidation rates, profile lipids via lipidomics, assess peroxisomal enzyme activities, and analyze metabolomic shifts. These assays help elucidate the mechanistic consequences of ACOT8 loss and its broader metabolic effects. For further details, please contact Ascent Research.
