The COX18 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene disruption product designed to ablate COX18 function in the Raji B lymphocyte lineage. This product is supplied as a polyclonal knockout cell population, containing a heterogeneous mixture of edited cells that collectively lack intact COX18 expression. The polyclonal format avoids clonal selection artifacts and provides a robust loss-of-function platform for studying mitochondrial complex IV assembly in a human lymphoma context.
The Raji host cell line was established from a Burkitt??s lymphoma patient and is characterized by an Epstein-Barr virus (EBV)-positive, lymphoblastoid phenotype. As a B lymphocyte model, Raji cells recapitulate key features of B cell malignancies and are widely employed in cancer metabolism and immunology research. The EBV-positive background further offers a unique setting to examine mitochondrial function in virally transformed lymphocytes.
COX18 encodes a mitochondrial inner membrane translocase essential for the insertion of the C-terminal tail of nascent cytochrome c oxidase subunit II (MT-CO2) into the inner membrane, a critical step in the assembly of the cytochrome c oxidase (complex IV) holoenzyme. COX18 functions within a network of assembly factors including COX20, COX14, COX16, SCO1, and SCO2, and is thought to work in concert with the TIM23 import machinery. Transcriptional regulation of COX18 is driven by upstream activators such as PPARGC1A (PGC-1??), NRF1, and GABPA, linking mitochondrial biogenesis programs to oxidative phosphorylation capacity. Disruption of COX18 impairs complex IV activity, leading to diminished electron transport chain function, reduced ATP production, and loss of mitochondrial membrane potential.
In the Raji B lymphocyte context, COX18 knockout is particularly relevant for dissecting the contribution of mitochondrial oxidative phosphorylation to lymphoma cell growth and survival. B cell lymphomas often exhibit altered metabolic dependencies, and defects in complex IV assembly can exacerbate mitochondrial dysfunction, potentially triggering cell death or metabolic reprogramming. This model enables the study of mitochondrial complex IV deficiency-like phenotypes within a disease-relevant cellular environment, providing insights into pathologies such as Leigh syndrome and cardioencephalomyopathy.
Researchers can utilize these polyclonal knockout cells in a broad range of assays, including Western blotting to monitor complex IV subunit levels, RT-qPCR for mitochondrial biogenesis markers, Seahorse respirometry to measure oxygen consumption rate, and flow cytometry-based assessment of mitochondrial membrane potential using TMRM. Additionally, co-immunoprecipitation and immunofluorescence facilitate examination of COX18 interactors and complex IV localization. The model is also suitable for screening therapeutic compounds aimed at rescuing mitochondrial function or for synthetic lethality studies in combination with metabolic stressors. For further inquiries or technical support, please contact Ascent Research.
