The CPT1A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated through targeted disruption of the CPT1A gene in the Raji B-lymphocyte cell line. This polyclonal pool offers a genetically heterogeneous loss-of-function model, enabling the study of CPT1A-dependent processes without clonal selection pressure. The knockout model provides a robust tool for investigating mitochondrial long-chain fatty acid oxidation in a human B-cell lymphoma context.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid cell line originally derived from a Burkitt lymphoma patient. Widely utilized as a model for human B-cell lymphoma and EBV biology, Raji cells exhibit characteristic B-lymphocyte features and are extensively employed in immunological and oncological studies. This cellular background is particularly relevant for exploring metabolic adaptations in aggressive B-cell malignancies.
CPT1A (carnitine palmitoyltransferase 1A) encodes the rate-limiting enzyme of mitochondrial long-chain fatty acid oxidation, catalyzing the conversion of long-chain acyl-CoAs to acylcarnitines for transport across the outer mitochondrial membrane. CPT1A activity is allosterically inhibited by malonyl-CoA and transcriptionally regulated by upstream factors including AMPK, PPARA, and PGC1A in response to insulin, glucagon, and long-chain fatty acids. Downstream, CPT1A-driven fatty acid oxidation modulates ATP and acetyl-CoA production, ketone body synthesis, and mTOR signaling. The enzyme interacts functionally with CPT2, carnitine-acylcarnitine translocase (CACT), and other outer mitochondrial membrane proteins. Consequently, CPT1A integrates signals within AMPK, PPAR, mTOR, and insulin signaling pathways to maintain energy homeostasis.
Disruption of CPT1A in Raji polyclonal cells abolishes the rate-limiting step of mitochondrial long-chain fatty acid oxidation, impairing lipid catabolism and altering cellular energy metabolism. In B lymphocytes, this knockout disrupts metabolic flexibility, potentially affecting proliferation, survival, and stress responses. Given the reliance of many lymphomas on oxidative metabolism, the CPT1A knockout Raji model is valuable for dissecting the role of fatty acid oxidation in B-cell lymphoma pathogenesis and for evaluating metabolic vulnerabilities.
This product is suitable for a wide range of applications including metabolic reprogramming studies in B-cell lymphoma, investigation of fatty acid oxidation in lymphocyte function, drug screening for CPT1A inhibitors, and cancer metabolism research. Researchers can validate knockout using Western blotting and RT-qPCR, and monitor functional consequences via fatty acid oxidation assays with radiolabeled palmitate, Seahorse mitochondrial stress tests, ATP measurements, and cell proliferation or apoptosis assays. This model also enables testing sensitivity to pharmacological inhibitors such as etomoxir. For further information or to inquire about custom configurations, please contact Ascent Research.
