The PFKL Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji Burkitt lymphoma B lymphocyte line, engineered for targeted disruption of the PFKL gene. PFKL encodes the liver-type phosphofructokinase, a rate-limiting enzyme of glycolysis that catalyzes the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate. This polyclonal knockout model provides a heterogeneous loss-of-function system, enabling robust investigation of PFKL-dependent glycolytic regulation without clonal artifacts. The product is supplied as a mixed population of edited cells, ensuring broad representation of gene disruption events for reliable phenotypic analyses.
Raji cells are an EBV-positive, tumorigenic B lymphocyte line derived from a patient with Burkitt lymphoma, widely utilized in immunology and oncology research. These cells exhibit a highly glycolytic phenotype characteristic of aggressive lymphomas, making them an ideal host for studying metabolic vulnerabilities. Their capacity for rapid proliferation and established role in antibody production further enhance their utility in cancer metabolism and B cell biology investigations. The Raji background provides a clinically relevant context for assessing PFKL function, given the dependence of Burkitt lymphoma on the Warburg effect and heightened glycolytic flux for survival and growth.
PFKL functions as a central node in cellular energy metabolism, integrating signals from upstream regulators including c-Myc, HIF-1??, and insulin signaling, while being allosterically modulated by AMP and citrate. The enzyme interacts directly with PFKFB and AMPK and cooperates with other PFK isoforms to govern glycolytic rate. Its activity drives the production of pyruvate, lactate, and ATP, and feeds into the pentose phosphate pathway to generate NADPH and ribose-5-phosphate for biosynthesis. In cancer cells, PFKL sustains the Warburg effect, wherein aerobic glycolysis supports rapid proliferation and biomass synthesis.
In the Raji Burkitt lymphoma model, PFKL knockout profoundly disrupts glycolytic flux, leading to reduced lactate secretion and diminished ATP production, thereby impairing the Warburg effect. This metabolic crisis is predicted to slow proliferation, enhance sensitivity to intrinsic apoptotic signals, and alter the balance of biosynthetic precursors required for nucleotide and lipid synthesis. The polyclonal knockout population reflects the heterogeneous metabolic adaptation observed in tumors, offering a physiologically relevant platform to dissect PFKL contributions to lymphoma maintenance and metabolic reprogramming.
This PFKL knockout model supports diverse research applications, including cancer metabolism studies, glycolysis inhibition investigations, and drug screening for metabolic inhibitors targeting the Warburg effect. Typical assays compatible with these cells encompass Western blotting and RT-qPCR for target validation, metabolic flux analysis using Seahorse technology, lactate quantification, proliferation measurements, and apoptosis detection. The polyclonal design facilitates high-throughput screening and functional genomics studies without the limitations of single-cell clones. For additional technical details or ordering inquiries, please contact Ascent Research.
