COQ8B Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which COQ8B has been disrupted to generate a loss-of-function model for coenzyme Q biosynthesis and mitochondrial research. Derived from the Raji B lymphocyte cell line, this product provides a heterogeneous pool of edited cells, enabling robust investigation of gene function without the bottleneck effects of clonal selection. The polyclonal format preserves cellular diversity, making it suitable for pooled screening and population-level analyses of metabolic and signaling phenotypes. The COQ8B gene disruption is achieved through CRISPR/Cas9-mediated targeting, yielding a versatile tool for studying the molecular consequences of impaired coenzyme Q synthome integrity.
The host Raji cell line is an Epstein-Barr virus-positive Burkitt’s lymphoma-derived model originating from an African patient, widely employed in immunology and cancer biology. As a B lymphocyte, Raji cells are instrumental in studying antigen presentation, B cell receptor signaling, and immune responses. Their robust proliferative capacity and well-characterized genetic background make them an ideal platform for gene-editing studies. In the context of COQ8B knockout, Raji cells provide a unique system to examine how mitochondrial energy metabolism influences B cell function, survival, and stress responses, complementing studies in non-immune cell models.
COQ8B encodes an atypical kinase-like protein that functions as a critical stabilizer of the CoQ synthome, a multi-subunit complex responsible for coenzyme Q10 biosynthesis. COQ8B interacts directly with COQ3, COQ4, COQ5, COQ6, COQ7, and COQ9, and its activity is regulated by upstream signals including PPARGC1A (PGC-1??) and cellular energy status. Downstream, COQ8B promotes the enzymatic steps mediated by COQ3, COQ5, COQ6, and COQ7, ultimately driving ubiquinone production. Disruption of COQ8B destabilizes the synthome, leading to diminished coenzyme Q levels, defective mitochondrial electron transport chain function, and reduced ATP synthesis, thus coupling energy metabolism to broader cellular processes.
Within the Raji B lymphocyte context, COQ8B knockout allows dissection of mitochondrial dysfunction in an immune-competent cellular environment. Given the reliance of lymphocytes on oxidative phosphorylation during activation and differentiation, this model is particularly relevant for studying how coenzyme Q deficiency impacts immune cell metabolism. The knockout cells can be used to explore links between mitochondrial energetics and B cell-mediated immunity, as well as to model aspects of primary coenzyme Q10 deficiency syndromes, including those with renal and neurological manifestations. Moreover, the model supports investigation of how COQ8B loss influences cell viability, proliferation, and sensitivity to metabolic stressors, offering a platform for therapeutic screening.
Detailed research applications include western blotting to confirm COQ8B protein loss and assess CoQ synthome components, HPLC-based quantification of coenzyme Q10 levels, Seahorse respirometry to evaluate mitochondrial oxygen consumption, ATP assays to gauge energy status, and flow cytometry for mitochondrial mass and membrane potential measurements. Viability assays under metabolic challenge further characterize phenotypic consequences. This knockout tool is suited for drug screening targeting CoQ deficiency and for fundamental studies of ubiquinone biology in a lymphocyte setting. For further information or technical support, please contact Ascent Research.
