The ACOX3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte cell line, offering a loss-of-function model for the peroxisomal acyl-CoA oxidase ACOX3. This polyclonal population provides a heterogeneous pool of gene-disrupted cells, enabling robust population-level studies of peroxisomal fatty acid ??-oxidation, reactive oxygen species (ROS) dynamics, and T-cell biology without clonal artifacts.
The Jurkat host cell line is an immortalized human T lymphocyte established from a 14-year-old acute T cell leukemia patient. Widely utilized in T-cell signaling and leukemia research, Jurkat cells exhibit rapid proliferation and well-defined pathways. Integrating ACOX3 knockout into this leukemic T-cell background facilitates the investigation of peroxisomal metabolism in immune cell function and malignant transformation.
ACOX3 encodes the peroxisomal enzyme that catalyzes the rate-limiting, FAD-dependent desaturation of 2-methyl branched-chain fatty acids, a critical step in phytanic acid degradation, producing a 2-enoyl-CoA intermediate and H2O2. Its expression is regulated by PPAR??, PPAR??, PPAR??, LXR, and PGC-1??. Downstream, the substrate is further processed by HSD17B4, ECH1, ACAA1, and SCP2 to yield acetyl-CoA and propionyl-CoA. Peroxisomal import of ACOX3 requires PEX5 and PEX7, and the enzyme interacts with FAD and catalase (CAT) for activity and ROS detoxification. Thus, ACOX3 sits at a nexus controlling branched-chain fatty acid metabolism and peroxisomal ROS generation.
Disruption of ACOX3 in Jurkat cells impairs the breakdown of 2-methyl branched-chain fatty acids, leading to altered lipid homeostasis and potential phytanic acid accumulation. The consequent changes in peroxisomal ROS may influence T-cell activation, proliferation, and apoptosis, processes central to leukemia cell maintenance. This model enables the exploration of metabolic vulnerabilities in leukemia and the study of ROS-mediated signaling in immune cells, contributing to the understanding of peroxisomal disorders.
The ACOX3 knockout Jurkat polyclonal cells support applications in peroxisomal disorder modeling, T-cell lipid metabolism, and drug sensitivity assays targeting fatty acid oxidation. Researchers can employ complementary assays including Western blotting and RT-qPCR for target validation, ACOX3 enzymatic activity assays, immunofluorescence for peroxisomal morphology, fatty acid oxidation measurements using radiolabeled or stable-isotope tracers, ROS assessment with fluorescent probes, cell proliferation and apoptosis kinetics, and metabolomic profiling to quantify acetyl-CoA, propionyl-CoA, and phytanic acid levels. For technical support and custom requests, please contact Ascent Research.
