The FADS1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal loss-of-function model disrupting the human FADS1 gene within the Raji B-lymphoblastoid cell line. This polyclonal knockout population abolishes expression of delta-5 desaturase, the enzyme responsible for introducing a cis double bond at the delta-5 position of long-chain polyunsaturated fatty acids, thereby blocking the conversion of dihomo-??-linolenic acid to arachidonic acid. The product provides a physiologically relevant human cell system for interrogating the metabolic and signaling consequences of impaired fatty acid desaturation in B-cell contexts.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B-lymphoblastoid line, widely used as a model for B-cell biology, EBV latency, and lymphoma pathogenesis. This suspension-adapted line retains key features of B-lymphocyte biology and permits robust genetic manipulation, making it suitable for CRISPR/Cas9-mediated knockout studies aimed at dissecting metabolic pathways underlying B-cell malignancies and immune functions.
FADS1 encodes delta-5 desaturase, a critical gatekeeper in the biosynthesis of arachidonic acid and eicosapentaenoic acid from essential fatty acid precursors. The enzyme functions within a multienzyme complex involving FADS2, ELOVL5, cytochrome b5, and NADH-cytochrome b5 reductase, and is transcriptionally regulated by SREBP1, PPAR-alpha, LXR, and insulin signaling in response to dietary fatty acids. Loss of FADS1 activity prevents formation of arachidonic acid, a precursor for eicosanoids including prostaglandins and leukotrienes, and alters membrane phospholipid composition, with downstream effects on inflammatory signaling networks and cellular lipid homeostasis.
In Raji cells, elimination of FADS1-derived arachidonic acid production disrupts the intrinsic capacity for eicosanoid synthesis, thereby attenuating autocrine and paracrine inflammatory loops that may influence lymphoma cell growth and the tumor microenvironment. Furthermore, altered membrane unsaturation can modulate ferroptosis susceptibility and EBV latency-associated metabolic demands, positioning these knockout cells as a tool for investigating metabolic vulnerabilities in B-cell lymphomas and the intersection of lipid metabolism with oncogenic signaling.
Researchers can employ this knockout model to perform functional studies of polyunsaturated fatty acid metabolism, lipidomic profiling via GC-MS or LC-MS, and quantification of arachidonic acid-derived mediators by ELISA. The cells are also suitable for ferroptosis induction assays, flow cytometric assessment of lipid peroxidation, and molecular analyses including RT-qPCR, western blotting, and Sanger sequencing for indel verification in the polyclonal population. For technical inquiries, contact Ascent Research.
