The ELOVL5 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphoblastoid cells, engineered for targeted disruption of the ELOVL5 gene. The polyclonal format yields a genetically diverse pool carrying ELOVL5 loss-of-function alleles, avoiding clonal artifacts and enabling pooled loss-of-function studies in lipid metabolism and B cell biology.
Raji is a human B lymphoblastoid cell line isolated from a Burkitt lymphoma. Growing in suspension and latently infected with EBV, Raji cells are widely used to study B cell receptor (BCR) signaling, apoptosis, and viral latency. Their malignant origin and rapid proliferation make them relevant for lymphoma research. As a suspension line, they are suitable for lipid extraction, high-throughput screening, and flow cytometric analysis of membrane properties.
ELOVL5 encodes a fatty acyl-CoA elongase that catalyzes elongation of C18 and C20 polyunsaturated fatty acyl-CoAs to C20 and C22 products, a step critical for biosynthesis of very long-chain omega-3 fatty acids such as docosahexaenoic acid (DHA) and docosapentaenoic acid (DPA). The enzyme functions downstream of FADS1 and FADS2 desaturases and cooperates with ELOVL2 and ELOVL4. Its transcription is activated by SREBP1 and PPAR??, and it responds to dietary PUFA availability and insulin. ELOVL5 interacts with fatty acid-binding proteins (FABPs) to channel substrates. The products serve as precursors for resolvins and protectins, lipid mediators that regulate inflammation. Disruption of ELOVL5 thus blocks conversion of eicosapentaenoic acid (EPA) to DHA, reshaping the cellular lipid profile.
In Raji cells, ELOVL5 knockout likely alters membrane phospholipid composition, lipid raft organization, and BCR signaling platforms. B cell lymphomas often exhibit reprogrammed lipid metabolism to sustain growth, and loss of ELOVL5 may disrupt membrane fluidity and production of pro-resolving mediators, impairing signal transduction. Moreover, EBV-positive Raji cells provide a context to study how viral latency intersects with lipid metabolism. Thus, this model enables dissection of ELOVL5??s role in lymphoma proliferation, drug response, and BCR-mediated activation.
Typical assays include Western blot and RT-qPCR for knockout confirmation, LC-MS/MS fatty acid profiling and lipidomics to characterize lipid species, and flow cytometry for membrane lipid composition. Functional studies span proliferation, apoptosis, drug sensitivity testing, and phospho-flow analysis of BCR signaling. The polyclonal pool is suited for genetic screens and complementation with wild-type ELOVL5. This product also supports research into spinocerebellar ataxia type 38 disease mechanisms. For further information, please contact Ascent Research.
