PFKM Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B lymphocyte cell line. The PFKM gene, encoding muscle-type phosphofructokinase, is disrupted to create a loss-of-function model for studying glycolysis and metabolic regulation. This polyclonal population retains genetic diversity typical of pooled editing, enabling robust and reproducible experiments without clonal bias.
Raji cells are a human Burkitt’s lymphoma B lymphocyte line, widely used as a model for B-cell biology, lymphomagenesis, and immune function. As lymphoblasts, they exhibit high proliferative capacity and active metabolic programs, making them particularly suitable for investigating glycolysis-dependent processes in hematological malignancies.
PFKM catalyzes the rate-limiting phosphorylation of fructose-6-phosphate to fructose-1,6-bisphosphate in glycolysis. It functions downstream of upstream regulators such as insulin, AMPK, HIF1A, and fructose-2,6-bisphosphate, and its activity is modulated by assembly into homotetramers or heterotetramers with PFKL and PFKP. PFKM-mediated flux generates downstream metabolites including fructose-1,6-bisphosphate, pyruvate, and ATP, linking it to energy production and anabolic pathways. In the glycolytic cascade, it acts in concert with HK2, GPI, ALDOA, GAPDH, PKM, and LDHA to coordinate glucose metabolism.
Ablation of PFKM in Raji cells impairs glycolytic flux, disrupting the balance between glycolysis and oxidative phosphorylation. This metabolic reprogramming can affect B-cell proliferation, survival, and effector functions, providing a platform to dissect the energy requirements of lymphoma cells. Given the association of PFKM mutations with Tarui disease (glycogen storage disease type VII), this knockout model also serves as a tool for studying metabolic myopathies in a lymphoid context, though care should be taken in extrapolating to muscle physiology.
This knockout model is suited for glycolysis research, B-cell metabolism studies, and lymphoma metabolic reprogramming investigations. Researchers can employ it in drug sensitivity assays to evaluate metabolic inhibitors, or in disease modeling of glycolytic defects. Representative assays include Western blotting to confirm PFKM loss, extracellular acidification rate (ECAR) measurement for glycolysis, ATP production assays, cell proliferation analysis, glucose uptake and lactate production quantification, and flow cytometry for metabolic markers. The polyclonal nature supports high-throughput screening and stable phenotypic characterization. For further technical details or ordering information, please contact Ascent Research.
