The DHRS7B Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte cell line, a well-characterized Burkitt lymphoma model. This heterogeneous cell pool carries targeted disruption of the DHRS7B gene, introduced via CRISPR/Cas9 genome editing without clonal selection, thus representing a robust loss-of-function system. By eliminating DHRS7B function, these cells enable investigation of short-chain dehydrogenase/reductase (SDR)-mediated steroid and retinoid metabolism in a B-cell context.
Raji cells originate from a male patient with Burkitt lymphoma and are persistently infected with Epstein-Barr virus (EBV), maintaining mature B-lymphocyte features. They serve as a key model for studying lymphomagenesis, immune signaling, and therapeutic drug responses. The male genetic background and EBV transformation provide additional dimensions for examining viral oncoprotein interactions and sex-specific metabolic profiles. Raji cells readily support proliferation, apoptosis, and metabolic flux assays, making them an ideal host for gene-editing applications.
DHRS7B encodes a NAD(P)+-dependent oxidoreductase that catalyzes redox reactions on steroid hormones and retinoids. Its catalytic activity is regulated by upstream nuclear receptors and cellular oxidative stress signals, positioning DHRS7B as a link between redox balance and lipid metabolism. Downstream, this enzyme modulates levels of steroid metabolites, retinoids, and other lipid derivatives, integrating into steroid hormone biosynthesis and retinol metabolism pathways. It directly interacts with NAD(P)+ cofactors and operates within the SDR superfamily, alongside CYP enzymes and retinol dehydrogenases, to fine-tune metabolic flux.
In the Raji B cell lymphoma model, knockout of DHRS7B allows researchers to dissect the functional role of steroid and retinoid metabolism in malignant B-cell behavior. Aberrant lipid metabolism and oxidative stress are hallmarks of lymphoma, and DHRS7B-deficient cells may exhibit altered proliferation, survival, and drug sensitivity. This model provides a platform to explore how DHRS7B-driven metabolic shifts influence oncogenic signaling and immune evasion in EBV-transformed B cells. Additionally, given the gene’s association with spermatogenic failure, studies may inform broader cellular oxidative defense and metabolic vulnerability mechanisms.
Key research applications include LC-MS-based steroid quantification, NAD+/NADH ratio measurement, MTT proliferation and Annexin V apoptosis assays, and drug sensitivity screening. Knockout verification is performed by RT-qPCR and Western blot. The polyclonal nature of this product makes it particularly suitable for population-level experiments that avoid clonal selection biases, providing a more physiologically relevant knockout model. For further technical details or experimental design support, please contact Ascent Research.
