The PEMT Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphocyte line, with targeted disruption of the PEMT gene. This heterogeneous pool of knockout cells facilitates loss-of-function analyses while avoiding clonal selection biases. Disruption of PEMT eliminates phosphatidylethanolamine N-methyltransferase activity, critical for de novo phosphatidylcholine synthesis from phosphatidylethanolamine. This model serves as a robust tool for probing lipid metabolism, membrane remodeling, and signaling in a B-cell lymphoma context.
Raji cells are an EBV-positive lymphoblastoid B cell line originally established from a male patient with Burkitt’s lymphoma. Widely utilized in immunological and lymphoma research, these cells exhibit characteristic features of transformed B lymphocytes, including high proliferative capacity and active metabolic pathways. The Raji background is particularly relevant for studying oncogenic signaling and metabolic adaptations in B-cell malignancies, as it retains key aspects of B-cell biology while offering experimental tractability. This host cell line thus provides an ideal platform for dissecting PEMT-mediated phosphatidylcholine synthesis in lymphoma cell function.
PEMT catalyzes the S-adenosylmethionine (SAM)-dependent methylation of phosphatidylethanolamine to produce phosphatidylcholine, a major membrane phospholipid and precursor for diacylglycerol (DAG) signaling. Its expression is regulated by estrogen, PPAR??, PGC-1??, FXR, SREBP-1c, and choline status, while its activity is influenced by the SAM/S-adenosylhomocysteine (SAH) ratio. Downstream, PEMT-derived phosphatidylcholine affects membrane phospholipid composition, VLDL secretion, and lipid droplet formation. In B-cell lymphoma, PEMT intersects with glycerophospholipid and choline metabolism pathways, which are often reprogrammed to sustain proliferation.
In Raji B cells, PEMT knockout disrupts a pivotal node in lipid biosynthesis, potentially impairing membrane integrity and altering oncogenic signaling cascades. Burkitt’s lymphoma cells depend on robust lipid metabolism for membrane biogenesis and energy homeostasis; thus, PEMT loss may sensitize them to metabolic stress and therapeutic interventions. This model allows researchers to dissect the metabolic dependencies of aggressive B-cell cancers and evaluate compensatory mechanisms that lymphoma cells employ to maintain lipid pools under disturbed conditions.
This product is suitable for a variety of assays including Western blotting, RT-qPCR, lipidomics (LC-MS), cell proliferation and apoptosis assays, flow cytometry, immunofluorescence, and RNA-seq. Applications range from studying PEMT??s role in B-cell lymphoma proliferation and survival, screening for lipid metabolism modulators, testing drug sensitivity under lipid metabolic stress, to exploring phosphatidylcholine-dependent signaling such as DAG-mediated pathways. The polyclonal knockout nature enables assessment of diverse editing outcomes and population-level effects. For additional technical information, please contact Ascent Research.
