The DERA Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the DERA gene in a human B-lymphoblastoid background. This polyclonal pool offers a heterogeneous collection of Raji cells carrying targeted disruptions in the DERA locus, generated via CRISPR/Cas9-mediated gene editing, and serves as a versatile model to investigate deoxyribose-phosphate aldolase function without the constraints of clonal variability or single-cell bottleneck effects. Researchers can employ this knockout population to explore the metabolic and proliferative consequences of DERA deficiency in a well-characterized B-cell lymphoma context.
The parental Raji cell line is an EBV-positive Burkitt lymphoma-derived B lymphoblastoid line that is widely utilized as a model system for B-cell biology. Raji cells exhibit hallmarks of adaptive immunity, including surface immunoglobulin expression, B cell receptor (BCR) signaling competence, and the ability to present antigens via MHC class II molecules. Their robust proliferation and well-defined signaling networks make them suitable for studying oncogenic processes, metabolic reprogramming, and the molecular basis of B-cell malignancies. The EBV-driven transformation status further provides a physiologically relevant platform for examining virus?Chost metabolic interactions.
DERA (deoxyribose-phosphate aldolase) encodes an enzyme that catalyzes the reversible aldol cleavage of 2-deoxy-D-ribose 5-phosphate into D-glyceraldehyde 3-phosphate and acetaldehyde. This reaction is a critical node connecting deoxyribonucleotide catabolism to the glycolytic and pentose phosphate pathways. DERA expression is transcriptionally regulated by c-MYC, E2F1, NRF2, and ATF4, linking its activity to oncogenic signaling, cell cycle progression, and oxidative stress responses. The glyceraldehyde-3-phosphate product feeds into glycolysis and the non-oxidative pentose phosphate pathway, where it is further processed by transketolase and transaldolase. Consequently, DERA activity influences dNTP pools, NADPH generation, and glycolytic intermediate levels, thereby supporting nucleotide salvage and redox balance. The loss of DERA disrupts deoxynucleotide salvage, potentially leading to altered nucleotide homeostasis and metabolic flux redistribution in proliferating cells.
In the Raji B-lymphoma context, where high proliferative demand necessitates robust nucleotide biosynthesis and metabolic flexibility, DERA knockout provides a means to dissect the relative contributions of the pentose phosphate pathway and deoxyribonucleoside salvage to cell growth and survival. Raji cells rely on c-MYC-driven metabolic reprogramming to sustain anabolism, and DERA sits downstream of this transcriptional network. Disruption of DERA is expected to impair the conversion of deoxyribose phosphates into glycolytic and pentose phosphate intermediates, possibly rendering the cells sensitive to nucleotide imbalances or oxidative stress. This model thus enables the investigation of metabolic vulnerabilities specific to B-cell lymphomas and the identification of potential targets for therapeutic intervention.
Key research applications include nucleotide metabolism studies, cancer metabolism research, functional genomics, drug target validation, and B-cell lymphoma modeling. The polyclonal knockout population can be characterized using Western blotting to confirm DERA protein loss, RT-qPCR for transcript-level confirmation, and Sanger sequencing to verify gene disruption at the genomic level. Metabolic consequences can be assessed through cell proliferation and viability assays, metabolic flux analysis, dNTP quantification, glycolytic rate measurements, and pentose phosphate pathway activity assays. This comprehensive toolkit supports mechanistic studies of DERA in oncogenic metabolism and the exploration of therapeutic strategies targeting nucleotide homeostasis in lymphoma. For further information, please contact Ascent Research.
