The CBR4 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBR4 gene. Derived from the Raji human B lymphocyte line, this product provides a loss-of-function model for investigating the mitochondrial and redox functions of CBR4. The polyclonal format ensures a heterogeneous population of gene-disrupted cells, suitable for pooled functional assays without clonal selection artifacts. This model is designed to facilitate studies on mitochondrial fatty acid synthesis and carbonyl detoxification pathways in a lymphocyte background.
Raji cells are an EBV-positive Burkitt’s lymphoma-derived B cell line that maintains a type III latency program, expressing key B cell markers CD19 and CD20. These cells serve as a well-established model for B cell malignancies, including non-Hodgkin lymphomas, and EBV-associated pathogenesis. Their robust proliferation and mitochondrial dependence make them particularly relevant for examining metabolic adaptations in cancer. The Raji background allows dissection of CBR4 functions within the context of aberrant B cell signaling and viral latency.
CBR4 encodes a mitochondrial 3-ketoacyl-ACP reductase that catalyzes NADPH-dependent reduction of 3-ketoacyl-ACP to 3-hydroxyacyl-ACP, a critical step in mitochondrial fatty acid synthesis (mtFAS). The mtFAS pathway, composed of MCAT, OXSM, CBR4, HTD2, and MECR, supplies octanoyl-ACP for lipoic acid biosynthesis. CBR4 also functions as a carbonyl reductase, detoxifying reactive lipid peroxidation products such as 4-hydroxynonenal. Its expression is regulated by the transcription factors NRF2 and PPAR?? in response to oxidative stress, and it interacts with the mitochondrial fatty acid synthase complex and acyl carrier protein, linking mtFAS to antioxidant defense.
Disruption of CBR4 in Raji cells impairs mtFAS, reducing lipoic acid synthesis and compromising pyruvate dehydrogenase and ??-ketoglutarate dehydrogenase activity, thus perturbing mitochondrial metabolism and TCA cycle flux. Loss of CBR4 also sensitizes cells to lipid peroxidation, increasing vulnerability to aldehyde cytotoxicity. Consequently, this knockout model helps elucidate how mitochondrial dysfunction and oxidative stress intersect in B cell malignancies and EBV latency.
Research applications include mitochondrial biology, redox regulation, cancer metabolism, and drug metabolism studies. CBR4 loss can be validated by western blot, RT-qPCR, and carbonyl reductase activity assays. Functional assessments encompass mitochondrial respiration, lipidomics profiling, oxidative stress challenge, and apoptosis assays ?? enabling dissection of mtFAS-dependent mechanisms in lymphomagenesis and neuroprotection. For technical inquiries, please contact Ascent Research.
