The EBP Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the EBP gene in the human Raji B lymphocyte line. This product provides a heterogeneous pool of knockout cells in which the target gene has been functionally inactivated through CRISPR/Cas9-mediated gene disruption, yielding a robust loss-of-function model for sterol metabolism research. The polyclonal format ensures broad representation of gene-edited cells without requiring single-cell clonal isolation, making it well-suited for population-level studies of cholesterol biosynthesis and its regulatory networks.
The Raji host cell line is an Epstein?CBarr virus (EBV)-positive Burkitt lymphoma-derived B lymphocyte line that grows in suspension and expresses the B cell markers CD20 and CD19. As a transformed lymphoblastoid line, Raji cells retain key features of mature B cells, including the capacity for antibody production and antigen presentation, while offering ease of genetic manipulation and scalability. This lineage provides a physiologically relevant background for investigating sterol metabolism in the context of B lymphocyte biology and associated malignancies.
The EBP gene encodes the sterol isomerase that catalyzes the conversion of zymostenol to lathosterol within the post-squalene cholesterol biosynthesis pathway. This enzyme operates downstream of well-characterized pathway components such as HMGCR, SQLE, LSS, CYP51A1, SC4MOL, and NSDHL, and upstream of DHCR7. EBP activity is tightly regulated by SREBP transcription factors in response to cholesterol homeostatic signals. Its protein partner sterol carrier protein 2 (SCP2) facilitates substrate channeling. Disruption of EBP consequently blocks the formation of lathosterol, 7-dehydrocholesterol, and ultimately cholesterol, leading to an accumulation of zymostenol and potentially compromising membrane integrity, lipid raft assembly, and steroidogenesis.
In Raji B cells, cholesterol is critical for maintaining plasma membrane fluidity, forming lipid rafts that support B cell receptor signaling, and enabling efficient antigen presentation and antibody secretion. By abolishing EBP isomerase activity, this knockout model disrupts the normal sterol profile, offering a unique system to explore how altered cholesterol biosynthesis affects transformed B lymphocyte functions. The model is particularly valuable for dissecting the roles of sterol intermediates in lymphoblastoid physiology and for linking sterol metabolism defects to immune cell dysfunction.
The EBP Knockout Raji Polyclonal Cells are suitable for a wide range of research applications, including cholesterol metabolism studies using radiolabeling assays or LC-MS steroid profiling, modeling of X-linked dominant chondrodysplasia punctata (Conradi-H??nermann syndrome), sterol pathway inhibitor screening, and drug metabolism or sensitivity testing. Representative experimental workflows include western blotting for EBP and downstream targets, RT-qPCR to assess pathway gene expression, immunofluorescence for protein localization, and flow cytometry for surface marker analysis. For additional details, please contact Ascent Research.
