The COQ9 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring target-gene disruption of the COQ9 locus within the Raji B-lymphocyte background. This product provides a heterogeneous pool of edited cells with loss of COQ9 function, enabling researchers to study the effects of COQ9 deficiency in a lymphoma-derived, EBV-positive model. The polyclonal format captures a broad spectrum of editing events without single-cell cloning, offering a practical tool for investigating mitochondrial coenzyme Q10 biology.
Raji cells are a suspension-adapted lymphoblastoid cell line originating from a Burkitt lymphoma patient and carry the Epstein?CBarr virus genome. These B lymphocytes are widely employed in immunology, hematology, and cancer biology due to their robust proliferation and capacity for antigen presentation and antibody secretion. Their transformed phenotype and mitochondrial dependency make them particularly suitable for examining metabolic perturbations and oncogenic signaling in the context of coenzyme Q deficiency.
COQ9 encodes a lipid-binding protein essential for coenzyme Q (ubiquinone) biosynthesis; it facilitates the delivery of a precursor lipid to COQ7 for ring hydroxylation, a critical step in ubiquinone maturation. The COQ9 protein functions within a multi-subunit complex that includes COQ4, COQ6, COQ7, COQ8A, and COQ8B, and its expression is regulated by transcription factors such as PPARGC1A, NRF1, NRF2, SREBF2, and PPARA. Disruption of COQ9 stalls ubiquinone synthesis, leading to reduced CoQ10 levels and impaired electron transport chain activity, which compromise mitochondrial membrane potential and ATP production while increasing reactive oxygen species, thereby sensitizing cells to ferroptosis.
In Raji lymphoma cells, COQ9 knockout creates a model of mitochondrial dysfunction directly relevant to primary coenzyme Q10 deficiency disorders, including mitochondrial encephalomyopathy, cerebellar ataxia, and nephrotic syndrome. The lymphoblastoid background allows investigation of how impaired oxidative phosphorylation influences B-cell receptor signaling, antigen presentation, and proliferative capacity. Moreover, the elevated oxidative stress and ferroptosis sensitivity in this model provide a valuable platform for testing therapeutic interventions aimed at restoring mitochondrial function or exploiting metabolic vulnerabilities in B-cell malignancies.
Researchers can employ these cells in a variety of functional assays: Western blotting and RT?qPCR to confirm COQ9 disruption, HPLC-based quantification of intracellular CoQ10 levels, Seahorse respirometry to assess oxygen consumption and glycolytic flux, ATP luminescence assays to gauge energy status, and flow-cytometric ROS detection to monitor oxidative stress. Proliferation assays and ferroptosis induction studies with viability readouts further enable screening of CoQ10 bypass therapies and exploration of ferroptosis-mediated cell death in lymphoma. For additional product details or customization options, please contact Ascent Research.
