The NADK2 Knockout Raji Polyclonal Cells provide a genetically disrupted model of the mitochondrial NADK2 gene in the human B lymphocyte lineage. This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji cells, offering a heterogeneous mixture of knockout alleles that collectively ablate NADK2 function. This loss-of-function system is well suited for studying mitochondrial NADP(H) metabolism and redox control in population-based assays without requiring single-cell cloning.
The Raji cell line is a human Burkitt’s lymphoma-derived B lymphocyte model extensively used in immunology and oncology. These cells retain antigen-presentation capacity and immunoglobulin production, recapitulating key features of B cell biology. Raji cells are widely employed to study B cell receptor signaling, apoptosis, and viral oncogenesis, and their rapid proliferation facilitates large-scale CRISPR editing and functional screening. This host system provides a physiologically relevant platform for investigating gene function in lymphoma and B lymphocyte-related contexts.
NADK2 encodes the mitochondrial NAD+ kinase that phosphorylates NAD+ to NADP+, the rate-limiting step in mitochondrial NADP(H) synthesis. NADPH generated by this reaction fuels the glutathione and thioredoxin antioxidant systems, maintaining redox homeostasis. NADK2 is regulated by NRF2, PGC-1??, and AMPK in response to oxidative stress and nutrient deprivation. It interacts with the mitochondrial inner membrane translocase and NAD+ transporters. Knockout of NADK2 disrupts mitochondrial NADPH production, altering the NADP+/NADPH ratio, suppressing glutathione reductase and thioredoxin reductase, and elevating mitochondrial ROS, thereby linking mitochondrial metabolism to redox signaling and stress adaptation.
In the Raji B lymphocyte model, NADK2 knockout dissects the role of mitochondrial NADPH metabolism in lymphoma biology. Rapidly proliferating lymphoma cells often depend on robust antioxidant systems to counteract oxidative stress. NADK2 loss exposes redox vulnerabilities specific to Burkitt’s lymphoma, potentially revealing metabolic dependencies that can be exploited for therapeutic intervention. This model is invaluable for investigating how mitochondrial NADPH deficiency affects survival during oxidative challenge, modulates apoptotic pathways, and alters the interplay between NAD metabolism and oncogenic signaling in B cell malignancies.
The NADK2 Knockout Raji Polyclonal Cells enable diverse functional analyses, including NADP+/NADPH ratio quantification, MitoSOX-based mitochondrial ROS detection, and cell viability tests under H2O2 or other oxidative challenges. Western blotting and RT-qPCR verify target-gene disruption, while metabolomics profiling uncovers metabolic reprogramming events. Key applications include investigating mitochondrial NADPH metabolism, dissecting redox signaling in lymphoma, and performing metabolic vulnerability screens in B cell cancers. This tool is suited for both mechanistic studies and drug-response assays. For further details, contact Ascent Research.
