PGLS Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphoblastoid cells designed to disrupt the PGLS gene, which encodes 6-phosphogluconolactonase. This knockout model provides a heterogeneous pool of edited alleles, enabling the investigation of PGLS loss-of-function effects on the pentose phosphate pathway (PPP) without clonal bias. The polyclonal format reflects the inherent genetic diversity achievable with CRISPR/Cas9-mediated gene disruption, making it suitable for studying population-level metabolic and signaling responses.
The Raji cell line, derived from a Burkitt??s lymphoma patient, is characterized by constitutive c-Myc overexpression and a highly proliferative B-cell phenotype. These lymphoblastoid cells retain key immunological features, such as surface immunoglobulin expression and antigen-presentation capacity, and are widely employed in studies of B-cell biology, lymphoma pathogenesis, and immune signaling. The Raji background provides a clinically relevant context to examine how metabolic enzyme disruption affects oncogenic processes.
PGLS catalyzes the hydrolysis of 6-phosphogluconolactone to 6-phosphogluconate, the second step of the oxidative PPP, acting directly downstream of glucose-6-phosphate dehydrogenase (G6PDH) and upstream of 6-phosphogluconate dehydrogenase (PGD). This reaction is essential for coupling glucose-6-phosphate oxidation to NADPH production and ribose-5-phosphate generation. PGLS expression is transcriptionally regulated by c-Myc and NRF2, linking PPP activity to oncogenic and oxidative stress programs, while p53 can transcriptionally restrain PPP flux. Disruption of PGLS therefore impairs NADPH-dependent redox balance and nucleotide precursor synthesis, key mediators downstream of PGLS activity.
In Raji cells, where c-Myc-driven metabolic reprogramming upregulates the PPP to support biosynthesis and maintain redox homeostasis, PGLS knockout is expected to severely compromise NADPH regeneration and ribose-5-phosphate availability. This likely sensitizes cells to oxidative stress, alters glutathione metabolism, and restricts nucleotide pools, creating a model to explore synthetic lethality approaches in MYC-driven lymphomas. The interaction between PGLS and upstream regulators such as c-Myc and NRF2, as well as downstream metabolites including NADPH and ribose-5-phosphate, underscores the pathway??s centrality in cancer metabolic adaptation.
Researchers can utilize PGLS Knockout Raji Polyclonal Cells to investigate metabolic dependencies in B-cell lymphoma through assays such as NADPH quantification, PPP flux analysis with 13C-glucose tracing, ROS detection, cell viability, and apoptosis under oxidative challenge. The model supports pharmacological screening for agents targeting PPP vulnerabilities and genetic complementation studies to dissect PGLS function. Additional applications include immunoblotting and qRT-PCR for PPP enzyme expression, flow cytometric analysis of oxidative stress markers, and drug sensitivity testing. For further product details or technical assistance, please contact Ascent Research.
