The COX15 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte line. This product disrupts COX15, which encodes an enzyme critical for heme A biosynthesis and cytochrome c oxidase assembly. The polyclonal format provides a heterogeneous cell pool, minimizing clonal artifacts and enabling robust functional studies of mitochondrial dysfunction in a human B cell context.
Raji is an EBV-positive Burkitt lymphoma cell line that retains B lymphocyte functions such as antibody production and antigen presentation. Its rapid suspension growth and experimental tractability make it ideal for studying B cell biology, lymphomagenesis, and immune responses, particularly in the context of mitochondrial metabolism.
COX15 catalyzes the final step in heme A biosynthesis, hydroxylating heme O to heme A, the prosthetic group of cytochrome c oxidase (Complex IV). This reaction is essential for Complex IV assembly and function within the electron transport chain. COX15 interacts with COX10, SURF1, SCO1, and SCO2 to coordinate heme A production and maturation of the oxidase. Transcriptionally, COX15 is regulated by PPARGC1A, NRF1, and TFAM, key drivers of mitochondrial biogenesis, and possibly by HIF1A. Loss of COX15 impairs oxidative phosphorylation, reduces ATP output, and alters ROS homeostasis, underlying mitochondrial complex IV deficiency disorders like Leigh syndrome.
B lymphocytes require robust mitochondrial respiration to support activation, proliferation, and antibody production. This COX15 knockout model enables dissection of how Complex IV deficiency impacts B cell metabolism, survival, and immune function. It is particularly valuable for studying metabolic reprogramming in lymphoma, where mitochondrial dysfunction may promote tumor progression and therapy resistance. The system also facilitates exploration of heme A biosynthesis in lymphoid malignancies and the interplay between mitochondrial signaling and B cell receptor pathways.
This polyclonal knockout model supports mitochondrial disease modeling, drug screening for mitochondrial disorders, and apoptosis research. Knockout validation can be performed by Western blot or RT-qPCR, while mitochondrial function is assessed via Seahorse mito stress tests and JC-1 flow cytometry. Complementary assays include ATP and ROS measurement, and Annexin V apoptosis detection. Immunofluorescence for cytochrome c oxidase subunits can monitor Complex IV assembly. The polyclonal format minimizes selection bias and provides a reliable platform for population-level metabolic studies. For further information, please contact Ascent Research.
