The MBOAT7 Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of human Raji B lymphocytes carrying targeted disruptions in the MBOAT7 gene. This heterogeneous knockout pool is designed for loss-of-function studies, avoiding clonal bias and enabling robust characterization of MBOAT7-dependent phenotypes. The polyclonal format provides a convenient and reproducible model for investigating phospholipid metabolism, inflammatory signaling, and B cell biology.
The Raji cell line is an EBV-positive lymphoblastoid line derived from a Burkitt’s lymphoma patient, widely used as a model of mature B lymphocytes. Raji cells express B cell surface markers, grow in suspension, and retain characteristics of transformed B cells, making them suitable for lymphoma research and signal transduction studies. This host background allows examination of lipid-mediated pathways in a clinically relevant B lymphocyte context.
MBOAT7 encodes a lysophosphatidylinositol (LPI) acyltransferase that catalyzes arachidonic acid transfer from arachidonoyl-CoA to LPI, forming phosphatidylinositol (PI). This reaction, part of the Lands cycle, is functionally linked to ACSL4-mediated arachidonic acid activation and PLA2-driven deacylation. MBOAT7 activity is regulated by transcription factors including SREBP1, PPAR??, and LXR. Disruption of MBOAT7 reduces arachidonoyl-PI pools, limiting substrate for PI3K/Akt/mTOR signaling and decreasing eicosanoid production (prostaglandins, leukotrienes). Consequently, the knockout model exhibits altered membrane phospholipid composition and dampened inflammatory signal transduction, reflecting the gene’s central role in phospholipid remodeling and lipid signaling.
In Raji B cells, MBOAT7 loss-of-function illuminates the intersection of lipid metabolism and oncogenic signaling. Impaired arachidonoyl-PI synthesis dysregulates PI3K/Akt activity, a pathway critical for B cell survival and lymphoma progression. Altered eicosanoid output may further influence the inflammatory microenvironment. This model thus provides a tool to study lipid-dependent mechanisms in B cell malignancies and extends to research on MBOAT7-related disorders such as NAFLD, metabolic syndrome, and alcohol-related liver disease, where phospholipid dysregulation is a hallmark.
Key applications include lipidomic profiling of PI species, Western blot analysis of PI3K/Akt phosphorylation, and ELISA-based eicosanoid quantification. Flow cytometry for B cell surface markers, cell viability assays under metabolic stress, and cytokine profiling further characterize knockout phenotypes. The model is suited for drug discovery targeting MBOAT7-associated metabolic and liver diseases, and for investigating B cell lymphoma lipid metabolism. For additional information or support, please contact Ascent Research.
