The NDUFS6 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the NDUFS6 gene in the human Raji B lymphoblast cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells carrying targeted mutations, and is suitable for investigating the biological consequences of mitochondrial Complex I deficiency.
The Raji cell line is an Epstein-Barr virus (EBV)-positive, CD19+ CD20+ human B lymphoblast that was originally derived from a Burkitt lymphoma and grows in suspension culture. As an immortalized B lymphocyte, Raji retains key features of malignant B-cell biology, including rapid proliferation and alterations in metabolic and survival pathways, making it a well-characterized model for lymphoma research and immunometabolism studies.
NDUFS6 encodes an essential subunit of mitochondrial Complex I, interacting with core components NDUFS1, NDUFS2, NDUFS3 and assembly factors NDUFAF1, NDUFAF2 to facilitate electron transfer from NADH to ubiquinone. Its expression is regulated by PGC-1??, NRF1, and TFAM, while HIF-1?? modulates energy metabolism under hypoxia. Disruption impairs Complex I assembly, blocking electron flow, decreasing the NADH:NAD+ ratio and dissipating the mitochondrial membrane potential. Resulting ATP reduction and ROS elevation activate AMPK, stabilize HIF-1??, and may trigger p53-dependent apoptosis via caspase-3/9.
In the Raji lymphoblast background, NDUFS6 knockout provides a clinically relevant platform to study the intersection of mitochondrial dysfunction and B-cell malignancy. Given that Burkitt lymphoma cells often rely on aerobic glycolysis, disruption of Complex I further compromises oxidative phosphorylation and forces a shift toward glycolytic metabolism. This model enables interrogation of metabolic plasticity, ROS-mediated signaling, and adaptive responses critical for identifying therapeutic vulnerabilities in EBV-driven lymphomas.
This polyclonal knockout cell population is highly suited for functional assays including Seahorse metabolic flux analysis of oxygen consumption rate, direct measurement of Complex I activity via NADH oxidation, and JC-1 mitochondrial membrane potential assessment. Additional applications encompass ROS detection with H2DCFDA, Western blot analysis of NDUFS6 and downstream effectors, Annexin V apoptosis assays, and MTT cell viability testing. The model also serves drug screening for mitochondrial dysfunction and immunometabolic research in lymphoma. For further information, please contact Ascent Research.
