The ACSF2 Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of the ACSF2 gene in Jurkat T lymphocytes. This heterogeneous loss-of-function model eliminates the need for single-cell cloning and is ideal for population-level studies of ACSF2-dependent mitochondrial fatty acid metabolism.
Jurkat cells are an immortalized human T lymphocyte line derived from a patient with acute T cell leukemia. Widely used in T cell signaling and apoptosis research, these cells are metabolically responsive and well-suited for investigating the intersection of immune function and metabolism.
The ACSF2 gene encodes a mitochondrial acyl-CoA synthetase that activates medium-chain fatty acids and their derivatives by catalyzing the formation of acyl-CoA thioesters. These substrates are essential for ??-oxidation and lipid biosynthesis. ACSF2 expression is regulated by peroxisome proliferator-activated receptors PPARA and PPARG, the coactivator PGC-1??, and insulin/glucagon signals. The acyl-CoA products feed into the carnitine shuttle via CPT1A and CPT2, entering the mitochondrial matrix where they undergo ??-oxidation mediated by enzymes including ACADM, HADHA, and HADHB. This process yields acetyl-CoA for the TCA cycle and supports electron transport chain activity. ACSF2 also interacts physically with mitochondrial metabolic enzymes and respiratory complexes. Consequently, ACSF2 disruption impairs medium-chain fatty acid catabolism, leading to decreased mitochondrial respiration, reduced ATP production, and accumulation of non-esterified fatty acids.
Within Jurkat T lymphocytes, ACSF2 knockout has significant immunometabolic consequences. T cell activation requires metabolic reprogramming that includes elevated glycolysis and fatty acid oxidation. Loss of ACSF2 limits the mitochondrial capacity to utilize medium-chain fatty acids, potentially compromising ATP generation and skewing the metabolic balance. This can impair proliferation, alter cytokine secretion, and enhance apoptosis susceptibility. As Jurkat cells model leukemic T cell behavior, this knockout system is valuable for probing metabolic vulnerabilities in T cell malignancies and the role of mitochondrial dysfunction in immune dysregulation.
This cell product is suitable for a broad range of metabolic and immunological studies. Functional assays such as Seahorse XF fatty acid oxidation and Mito Stress tests allow direct measurement of mitochondrial respiratory parameters. Metabolomic profiling via LC-MS can quantify acyl-CoA species, while RT-qPCR and Western blotting validate changes in ACSF2 and downstream targets. Flow cytometry and apoptosis assays provide additional phenotypic readouts. Key research applications include mitochondrial biology, cancer metabolism, metabolic disorders, and T cell immunometabolism. For technical inquiries or additional details, please contact Ascent Research.
