The PEX3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population carrying disruptive mutations in the PEX3 gene, generated in the Raji B-lymphocyte cell line. This pool of gene-edited cells provides a loss-of-function model to study PEX3-dependent processes without clonal selection, capturing varied mutation events. The polyclonal format is advantageous for population-based assays such as biochemical profiling and drug screening. It enables direct investigation of peroxisomal biology in a human lymphoid background.
Raji is an EBV-positive Burkitt’s lymphoma-derived B-lymphoblastoid cell line widely used for B-cell malignancy research. These suspension-adapted cells retain B-cell features, including surface immunoglobulin expression and constitutive NF-??B activity driven by latent EBV proteins. Their rapid growth and ease of culture make them suitable for genetic manipulation. Introducing a PEX3 knockout into Raji cells allows the exploration of peroxisomal function in the context of B-cell lymphoma metabolism and survival signaling.
PEX3 encodes a peroxisomal membrane protein essential for peroxisome biogenesis, acting as a membrane anchor for the PEX19?Ccargo complex to facilitate insertion of peroxisomal membrane proteins (PMPs). Upstream regulators include PEX19 and PEX16; PEX3 interacts with PEX19, PEX16, and PMP34. It is required for membrane integration of downstream targets such as PMP70, PEX14, PEX13, and PEX10. Within the import pathway, PEX3 operates alongside PEX5 and PEX7 receptors. Disruption of PEX3 abolishes PMP insertion, resulting in empty ghost peroxisomes and defective matrix protein import, thereby crippling fatty acid beta-oxidation and plasmalogen synthesis.
In B-cell lymphomas, lipid metabolism is often reprogrammed, and peroxisomes contribute to very-long-chain fatty acid breakdown and ether lipid production. The PEX3 knockout Raji polyclonal model enables bulk analysis of metabolic alterations, lipidomic changes, and drug responses without clonal artifacts. Because Raji cells are EBV-transformed, this system can also be used to study whether latent viral factors influence peroxisomal activity or whether peroxisome loss alters viral latency or immune evasion. It provides a human cell platform for peroxisomal disorder pathology.
This knockout product supports multiple assays: immunofluorescence microscopy for PMP70 and PEX14 mislocalization, immunoblotting for PEX3 loss, peroxisomal beta-oxidation and plasmalogen synthesis measurements, subcellular fractionation, and electron microscopy of ghost peroxisomes. It serves as a disease model for Zellweger spectrum disorders and a tool for drug screening to rescue peroxisomal function. For technical inquiries or further information, contact Ascent Research.
