The ACSL5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T-lymphocyte line, designed for in vitro functional studies of ACSL5. This product provides a heterogeneous pool of cells with targeted disruption of the ACSL5 gene, enabling investigation of its role in lipid metabolism and energy homeostasis without selection for a single clonal variant. The polyclonal format minimizes artifacts arising from clonal selection while maintaining representation of diverse editing outcomes, making it suitable for population-level studies of gene function.
Jurkat cells are an immortalized human T-cell line originally isolated from the peripheral blood of a patient with acute T-cell leukemia. They proliferate in suspension as lymphoblasts and are extensively employed in T-cell signaling, activation, and apoptosis research. Jurkat cells exhibit robust metabolic plasticity, allowing detailed analysis of pathways linking lipid metabolism to immune cell function and malignant transformation. Their well-characterized signal transduction machinery, including TCR-mediated NFAT and NF-??B pathways, makes them a versatile platform for examining how metabolic alterations influence T-cell biology.
ACSL5 (Acyl-CoA Synthetase Long Chain Family Member 5) catalyzes the ATP-dependent activation of long-chain fatty acids to acyl-CoA thioesters, a critical step for channeling fatty acids into ??-oxidation, phospholipid and triglyceride synthesis, and ceramide production. ACSL5 is transcriptionally regulated by PPAR??, SREBP1c, insulin, and LXR, and it physically interacts with fatty acid transport proteins and other ACSL isoforms. Its product, acyl-CoA, serves as a substrate for CPT1A in the mitochondrial ??-oxidation pathway and allosterically modulates AMPK and PPAR?? signaling, thereby integrating nutrient availability with cellular energy balance. Knockout of ACSL5 disrupts this activating step, impairing fatty acid utilization and altering membrane lipid composition and signaling lipid pools.
In Jurkat T cells, ACSL5 knockout provides a physiologically relevant model for studying the intersection of fatty acid metabolism and immune cell function. Jurkat cells rely on glycolytic and oxidative metabolism to sustain proliferation and effector responses; disruption of ACSL5 perturbs the supply of activated fatty acids, potentially reducing ??-oxidation flux and shunting unused fatty acids toward storage or alternative pathways. This model can reveal metabolic vulnerabilities associated with T-cell leukemia and the role of ACSL5 in lipid-mediated signaling events, such as those involving ceramides and diacylglycerols, which influence apoptosis and proliferation. The polyclonal knockout population reflects the heterogeneity of gene inactivation, allowing assessment of dose-dependent metabolic effects.
This ACSL5 knockout model is highly suited for mechanistic studies in fatty acid metabolism, metabolic disease modeling, and cancer metabolism research. Investigators can perform fatty acid oxidation assays using 14C-palmitate or Seahorse flux analysis, ATP measurements, and lipid uptake assays with BODIPY-labeled fatty acids analyzed by flow cytometry. Mass spectrometry-based lipidomics enables detailed profiling of acyl-CoA species, triglycerides, and phospholipids. Western blotting and RT-qPCR can validate ACSL5 disruption and quantify downstream targets such as CPT1A, ACACA, and FASN. These applications support drug screening for obesity, type 2 diabetes, non-alcoholic fatty liver disease, and metabolic syndrome, as well as studies of immune cell metabolism. For further information or technical support, please contact Ascent Research.
