The PFKFB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the PFKFB2 gene across a heterogeneous pool of Raji B lymphocytes. This loss-of-function model avoids clonal biases and enables robust functional studies by capturing diverse editing events, enhancing reproducibility in metabolic and oncogenic research.
Raji cells are a suspension B-lymphocyte line derived from a Burkitt lymphoma patient and are Epstein-Barr virus (EBV)-positive. They retain B-cell functions such as antibody production and antigen presentation while exhibiting transformed proliferation. This makes them a highly relevant system for investigating glycolytic reprogramming and lymphomagenesis, providing a disease-relevant context for PFKFB2 studies.
PFKFB2 encodes a bifunctional enzyme that produces fructose-2,6-bisphosphate (F2,6BP), an allosteric activator of phosphofructokinase-1 (PFK-1), the rate-limiting glycolytic enzyme. PFKFB2 is activated by AMPK- and AKT-mediated phosphorylation and is transcriptionally upregulated by HIF-1?? under hypoxia, while it is inhibited by glucagon and protein kinase A. F2,6BP binds PFK-1 to relieve ATP inhibition and enhance glycolytic flux, increasing lactate production and glycolytic intermediates. PFKFB2 also interacts with 14-3-3 proteins and functions as a dimer. Thus, PFKFB2 integrates signals from energy stress (AMPK), growth factors (PI3K/AKT), and hypoxia (HIF-1??) to control glycolysis outcome.
In Raji B cells, PFKFB2 likely sustains the high glycolytic rate required for rapid proliferation and supports EBV-driven metabolic reprogramming. Disruption of PFKFB2 is expected to lower F2,6BP, reduce PFK-1 activity, and attenuate glycolytic flux, potentially impairing ATP supply and biosynthesis. This may render cells vulnerable to energy stress, triggering apoptosis or growth inhibition. This model thus allows dissection of PFKFB2??s role in Burkitt lymphoma metabolism and identification of compensatory pathways.
Applications include glycolysis stress tests via Seahorse analysis, lactate measurement, and fructose-2,6-bisphosphate quantification. The cells are also suitable for western blotting, RT-qPCR, proliferation, apoptosis, and flow cytometry assays. This knockout model supports cancer metabolism studies, glycolysis inhibition experiments, B-cell lymphoma research, metabolic reprogramming investigations, and drug target validation. For more information, please contact Ascent Research.
