The PGM5 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited heterogeneous Raji cell population designed to eliminate functional PGM5 expression. As a polyclonal knockout product, it provides a loss-of-function model that captures the genetic variability inherent in tumor cell populations, making it suitable for robust metabolic and oncological studies. This product enables researchers to dissect the role of phosphoglucomutase 5 in glucose handling and glycogen homeostasis within a B-lymphoma context.
Raji cells are an EBV-positive B lymphoblastoid line derived from a Burkitt lymphoma patient, growing in suspension. They serve as a well-established model for B-cell receptor signaling, humoral immunity, and B-cell malignancies. These cells exhibit c-Myc-driven proliferation and metabolic adaptations typical of aggressive lymphomas, offering a relevant platform to study how EBV and host metabolic pathways intersect.
PGM5 catalyzes the reversible conversion of glucose-1-phosphate to glucose-6-phosphate, a pivotal step in glycogen synthesis, glycolysis, and the pentose phosphate pathway. Its activity is regulated by c-Myc, insulin signaling, and HIF1A, and it homodimerizes, interacting with glycogenin and other phosphoglucomutases like PGM1. Downstream, PGM5 modulates levels of glucose-6-phosphate, glycogen, glycolytic intermediates, and pentose phosphate pathway metabolites. Disruption of this node is expected to impair glycogen accumulation and glycolytic flux, affecting energy production and biosynthetic processes.
In Raji lymphoma cells, PGM5 knockout likely compromises glycogen synthesis and glucose utilization, potentially reducing lactate output and altering cellular energy balance. This may sensitize cells to metabolic stress and influence BCR-dependent survival signals. Although PGM5 is not strongly linked to disease, its role in dilated cardiomyopathy is under investigation. The knockout model thus enables exploration of phosphoglucomutase function in lymphoma metabolic reprogramming and evaluates glycogen metabolism as a therapeutic target.
Researchers can validate PGM5 disruption via Western blot and RT-qPCR, and assess metabolic consequences using glycogen content assays, 2-NBDG glucose uptake, lactate production, and CellTiter-Glo viability tests. Transcriptomic profiling by RNA-seq and apoptosis analysis by flow cytometry further characterize the knockout phenotype. Primary applications encompass metabolic reprogramming in B-cell lymphomas, glycobiology of lymphoproliferative diseases, and drug screening targeting glucose metabolism. For protocol support or customization, please contact Ascent Research.
