The ECHDC3 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the ECHDC3 gene has been disrupted in the Raji human B lymphocyte cell line. This loss-of-function model enables investigation of the mitochondrial enoyl-CoA hydratase ECHDC3 and its involvement in fatty acid ??-oxidation within a Burkitt lymphoma-derived background. The polyclonal format preserves heterogeneous genetic modifications across the cell population, making it suitable for pooled functional assays and metabolic screening studies.
Raji cells originate from a patient with Burkitt lymphoma, an aggressive B-cell malignancy, and serve as a widely used model for studying B-cell biology, lymphoma pathogenesis, and immune system signaling. These suspension-adapted lymphoblastoid cells express B-cell surface markers and exhibit rapid proliferation. Their metabolic reliance on both glycolysis and oxidative phosphorylation renders them particularly useful for dissecting metabolic adaptations in cancer.
ECHDC3 encodes an enoyl-CoA hydratase that catalyzes the second step of mitochondrial fatty acid ??-oxidation, converting enoyl-CoA esters to 3-hydroxyacyl-CoA. This enzyme is transcriptionally regulated by PPAR??, PPAR??, and PGC-1??, which coordinate lipid metabolism programs. ECHDC3 associates with the mitochondrial trifunctional protein complex, directly interacting with HADHA and HADHB, and functions downstream of ECHS1. Its activity contributes to the generation of acetyl-CoA, NADH, and ATP, ultimately feeding the TCA cycle. Disruption of ECHDC3 therefore blocks the ??-oxidation pathway, leading to impaired energy production from fatty acids and potential accumulation of upstream lipid intermediates.
In the Raji cellular context, ECHDC3 loss is expected to perturb lipid catabolism and force a metabolic shift that may reveal targetable vulnerabilities in B-cell lymphoma. Burkitt lymphoma cells often exhibit upregulated fatty acid oxidation, and ablation of ECHDC3 can uncover dependencies on mitochondrial ??-oxidation for proliferation and survival. This model thus provides a platform for dissecting how lymphoma cells balance lipid metabolism under varying nutrient conditions and for evaluating metabolic inhibitors that target compensatory pathways.
Typical applications include metabolic flux analysis using Seahorse instrumentation, direct measurement of fatty acid oxidation rates, and immunoblotting of ??-oxidation enzymes to confirm pathway disruption. Complementary lipidomic profiling can trace changes in acyl-carnitine and TCA cycle intermediates, while RT-qPCR enables assessment of transcriptional responses of metabolic genes. Cell proliferation, viability, and apoptosis assays further define the functional consequences of ECHDC3 deficiency. For detailed experimental protocols, technical validation data, and ordering information, please contact Ascent Research.
