The NDUFV3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B-lymphoblastoid cell line. This product features disruption of the NDUFV3 gene, which encodes a critical subunit of mitochondrial complex I (NADH:ubiquinone oxidoreductase). The polyclonal population includes a diverse array of NDUFV3-edited alleles, providing a robust loss-of-function model without clonal selection. As a polyclonal population, it is suited for bulk studies rather than single-cell analyses.
Raji cells are an EBV-positive Burkitt lymphoma line characterized by a t(8;14) translocation that brings the c-MYC oncogene under the control of immunoglobulin enhancers, leading to its overexpression. This B-lymphoblastoid cell line is widely employed to study B-cell biology, Epstein-Barr virus latency mechanisms, and oncogenic transformation. The cells express surface markers typical of mature B cells and maintain latency III EBV gene expression programs, making them a relevant model for EBV-associated lymphomagenesis.
NDUFV3 is a core subunit of the NADH:ubiquinone oxidoreductase (complex I), where it contributes to the structural integrity and electron transfer activity of the enzyme. Its expression is regulated by key mitochondrial biogenesis factors including PPARGC1A (PGC-1??), NRF1, NRF2, and the estrogen-related receptor ESRRA (ERR??). Within complex I, NDUFV3 interacts with other subunits such as NDUFS1, NDUFS2, NDUFV1, and NDUFV2, as well as assembly factors NDUFAF1 and NDUFAF2. Disruption of NDUFV3 leads to impaired oxidative phosphorylation, reduced ATP synthesis, and heightened reactive oxygen species production. Downstream, this metabolic dysfunction activates AMPK and stabilizes HIF-1??, while also triggering ASK1/JNK-mediated apoptosis and upregulating glycolytic enzymes including HK2 and LDHA.
In the Raji B-cell context, NDUFV3 knockout imposes a profound metabolic reprogramming by forcing a shift from oxidative phosphorylation to glycolysis. The combined effect of NDUFV3 loss and c-MYC overexpression exacerbates glycolytic dependency, mimicking the Warburg effect observed in many cancers. This engineered metabolic stress can influence cell survival, proliferation, and the maintenance of EBV latency, offering a unique platform to dissect the interplay between mitochondrial dysfunction and viral oncogenesis. The polyclonal nature of the population captures heterogeneous responses, which may better recapitulate physiological variability compared to single-cell clones.
This knockout model is suitable for mechanistic studies of mitochondrial complex I deficiency, metabolic reprogramming in B-cell lymphoma, and drug sensitivity profiling with complex I inhibitors such as metformin. The model supports Western blot analysis of NDUFV3 and complex I subunits, Seahorse-based oxygen consumption rate measurement, ATP luminescence assays, mitochondrial membrane potential assessment with JC-1, ROS detection by H2DCFDA or MitoSOX, lactate production measurement, and cell viability/apoptosis analysis by Annexin V/PI flow cytometry. It additionally enables flow cytometric cell cycle analysis, c-MYC expression profiling, and EBV gene expression studies. For technical inquiries, contact Ascent Research.
