The OSBPL3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji human B lymphocyte line, in which the OSBPL3 gene has been disrupted to create a loss-of-function model. Supplied as a heterogeneous cell pool, this product avoids clone-specific artifacts and provides a robust system for interrogating OSBPL3-dependent processes without the confounding effects of clonal selection. The polyclonal format enables researchers to assess average gene-disruption effects in a background closely resembling the parental line.
Raji cells are a well-established Burkitt’s lymphoma-derived B-cell line that is positive for Epstein-Barr virus (EBV) and carries a characteristic MYC translocation. These genetic drivers render Raji cells highly proliferative and widely used for studying B-cell malignancies, oncogenic signaling, chemotherapeutic responses, and viral lymphomagenesis. Their lymphoid origin makes them particularly relevant for investigating pathways that integrate lipid metabolism with immune cell function and cancer cell survival.
OSBPL3 (oxysterol-binding protein-like 3) acts as a non-vesicular lipid transporter that shuttles oxysterols and phosphatidylinositol-4-phosphate (PI4P) between the endoplasmic reticulum and other organelles, including the Golgi apparatus and plasma membrane. It is a central regulator of cholesterol homeostasis and PI4P-dependent signaling. OSBPL3 directly binds VAPA/VAPB at membrane contact sites and is transcriptionally controlled by sterol regulatory element-binding proteins (SREBPs) and liver X receptors (LXRs). Downstream, OSBPL3 influences the mTOR/AKT signaling axis and Golgi PI4P dynamics, thereby coupling lipid distribution to cell growth, proliferation, and survival. Through these interactions, OSBPL3 coordinates membrane composition with broader metabolic and oncogenic programs.
In the context of Raji B lymphoma cells, loss of OSBPL3 is expected to disrupt intracellular trafficking of cholesterol and oxysterols, leading to altered plasma membrane lipid raft organization and impaired B-cell receptor (BCR) signaling. Given that mTOR/AKT pathways are frequently hyperactivated in lymphomas and depend on proper lipid environments, OSBPL3 knockout may attenuate proliferative and anti-apoptotic signals. This model provides a valuable platform for elucidating how lipid homeostasis intersects with oncogenic cascades in B-cell malignancies and may reveal synthetic lethal vulnerabilities associated with MYC-driven lymphomas or lipid-targeted therapies.
This polyclonal knockout cell population is suited for lipid quantification (cholesterol and oxysterols), western blot analysis of OSBPL3 and signaling proteins (e.g., phospho-AKT, mTOR), cell proliferation and apoptosis assays, and drug sensitivity testing with statins. RNA sequencing can reveal transcriptomic changes in lipid metabolism genes, while flow cytometry assesses membrane lipid composition. The cells also facilitate screening for compounds targeting OSBPL3-deficient lymphomas. For technical details or ordering, contact Ascent Research.
