The PEX16 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human Raji B lymphocytes, with targeted disruption of the PEX16 gene. This loss-of-function model permits investigation of peroxisome biogenesis and metabolic functions in a lymphoid cell context, avoiding clonal selection biases inherent to monoclonal lines.
Raji host cell line is an EBV-positive Burkitt??s lymphoma B cell line that serves as a lymphoblastoid model for B cell biology and immune responses. Raji cells are well-characterized and easily cultured in suspension, facilitating a wide range of biochemical and imaging techniques. Their B cell origin allows unique studies on peroxisome-dependent processes in immune cells.
PEX16 is a peroxisomal membrane protein indispensable for early peroxisome assembly. It mediates the recruitment of PEX3 to nascent peroxisomes, enabling the import of membrane and matrix proteins. PEX16 interacts with PEX3, PEX19, and is connected to PEX11?? and PEX14, while its downstream effects govern peroxisomal enzyme activity and proliferation. Expression of PEX16 is transcriptionally controlled by PPAR??, PPAR??, and PGC-1??. CRISPR/Cas9-mediated PEX16 disruption blocks PEX3 recruitment, leading to defective import of peroxisomal proteins and loss of essential metabolic functions such as very long-chain fatty acid beta-oxidation, ether lipid synthesis, and bile acid metabolism.
In the Raji context, PEX16 knockout creates a model to dissect peroxisome biology in B lymphocytes. Peroxisomal dysfunction is causally linked to Zellweger spectrum disorders, neonatal adrenoleukodystrophy, and infantile Refsum disease. The Raji KO polyclonal population enables exploration of how peroxisomal deficiency alters immune cell physiology, including lipid mediator production, oxidative stress management, and malignant B cell behavior.
This product is ideal for studying peroxisome biogenesis, modeling inherited peroxisomal disorders, and drug screening for peroxisome-restorative compounds. Standard assays include immunofluorescence for catalase and PMP70, Western blotting for PEX16, PEX3, and PEX19, RT-qPCR of PEX genes, very long-chain fatty acid oxidation assays, and plasmalogen synthesis measurements. Cellular stress responses can also be profiled. For further information, please contact Ascent Research.