The OXCT1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Raji B lymphoblastoid line, with targeted disruption of the OXCT1 gene. This heterogeneous pool of edited cells, generated via CRISPR/Cas9-mediated gene disruption, avoids clonal selection biases and provides a robust system for studying OXCT1 loss-of-function in a B lymphocyte background, suitable for functional genomics and metabolic research.
Raji is an EBV-positive Burkitt lymphoma-derived B cell line that retains antibody production capacity and models adaptive immunity. Its transformed phenotype, driven in part by Epstein-Barr virus, offers a physiologically relevant setting to investigate metabolic dependencies in lymphomagenesis, making it an ideal host for examining the interplay between B-cell biology and metabolic regulation.
OXCT1 encodes succinyl-CoA:3-oxoacid CoA-transferase (SCOT), the rate-limiting enzyme of ketolysis that converts acetoacetate and succinyl-CoA to acetoacetyl-CoA and succinate. Transcription of OXCT1 is activated by PPAR?? and fasting signals, and suppressed by insulin and glucocorticoids, integrating hormonal and nutritional cues. The enzyme functions upstream of acetyl-CoA and TCA cycle entry, working alongside ACAT1, HMGCS2, BDH1, and HMGCL within the ketone body utilization pathway. Its activity depends on succinyl-CoA and acetoacetate as co-substrates. Knockout of OXCT1 abolishes ketone body oxidation, forcing a metabolic shift to glycolysis or alternative fuels.
In the Raji lymphoma model, OXCT1 knockout enables dissection of ketone metabolism??s role in B-cell malignancies. Aggressive lymphomas may exploit metabolic flexibility, including ketone body oxidation, to support proliferation and survival under nutrient stress; disrupting OXCT1 unmasks dependencies on glycolysis or glutaminolysis. This polyclonal knockout population thus serves as a critical tool for studying metabolic reprogramming, ketoacidosis-related pathology, and the functional significance of ketolysis in cancer, directly addressing how B-cell tumors adapt to fluctuating energy substrates.
Researchers can utilize these OXCT1 polyclonal knockout cells in a range of functional assays: RT-qPCR and western blotting validate gene disruption, Seahorse-based oxygen consumption rate (OCR) measurements assess mitochondrial respiration, ketone body consumption assays quantify ketolytic capacity, and cell viability assays under metabolic stress reveal adaptive responses. Metabolomics profiling of TCA cycle intermediates further defines the metabolic consequences of OXCT1 loss. These applications facilitate investigations into metabolic reprogramming in B-cell malignancies, the contribution of ketone metabolism to lymphoma survival, ketoacidosis disorder modeling, and therapeutic targeting of OXCT1 in cancer. For ordering or technical support, contact Ascent Research.
