The GPD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the GPD2 gene in Jurkat cells. The product consists of a heterogeneous pool of cells with GPD2 gene disruptions, generated by CRISPR/Cas9-mediated editing without single-cell cloning. This format preserves diverse editing outcomes, providing a robust model for loss-of-function studies in T lymphocyte biology and leukemic metabolism. The polyclonal approach avoids clonal selection bias and enables high-throughput screening of mitochondrial function and signaling pathways.
Jurkat cells, a human T lymphoblast-like line from an acute T cell leukemia patient, serve as a widely used model for TCR signaling, T cell activation, and leukemic transformation. Their immortalized, suspension-adapted growth facilitates large-scale genetic manipulation and metabolic assays. The well-characterized signaling nodes in Jurkat cells, including NFAT, NF-??B, and MAPK pathways, offer a defined context for studying the impact of metabolic gene knockouts on immune cell function and leukemia biology.
GPD2 encodes mitochondrial glycerol-3-phosphate dehydrogenase, an integral enzyme of the glycerol phosphate shuttle. It catalyzes the oxidation of glycerol-3-phosphate to dihydroxyacetone phosphate using FAD as a cofactor, transferring electrons to ubiquinone and driving ATP synthesis via the electron transport chain. GPD2 is regulated by thyroid hormone (T3), insulin, PPAR??, and CaMKII. Downstream, it influences FADH2 production, ubiquinone reduction, ATP output, and reactive oxygen species levels. The shuttle, with cytoplasmic GPD1, regenerates NAD+ from NADH, linking glycolysis to oxidative phosphorylation. Disruption of GPD2 impairs electron flow and redox balance, disrupting mitochondrial respiration.
In Jurkat T cells, GPD2 knockout models the consequences of a disrupted glycerol phosphate shuttle on T cell metabolism and leukemic survival. T cell activation triggers metabolic reprogramming, and GPD2 loss compromises mitochondrial ATP production and increases ROS, which can affect proliferation and activation. This system allows dissection of how mitochondrial dysfunction alters T cell effector functions and malignant growth, revealing compensatory pathways that sustain leukemia cells under impaired respiration. Such models are critical for identifying metabolic vulnerabilities in acute T cell leukemia.
These polyclonal knockout cells are ideal for investigating mitochondrial energy metabolism in T cells, metabolic reprogramming in leukemia, and screening for metabolic disorder therapeutics. Assays such as Seahorse metabolic flux analysis, ATP bioluminescence, ROS detection, and mitochondrial membrane potential measurements can be performed. Western blotting and RT-qPCR confirm GPD2 knockout, while apoptosis and metabolomics studies reveal downstream effects. The model supports research into type 2 diabetes, obesity, and metabolic syndrome by evaluating glycerol phosphate shuttle contributions to insulin secretion and redox regulation. For further details, contact Ascent Research.
