OSBPL2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the OSBPL2 gene has been disrupted, providing a heterogeneous loss-of-function model in a human B lymphoblast background. This product consists of a pool of cells carrying diverse genetic modifications at the OSBPL2 locus introduced by CRISPR/Cas9-mediated gene disruption, without clonal isolation. The polyclonal format allows researchers to study overall gene function while avoiding clone-specific artefacts, and it is ideal for experiments where average population responses are relevant. This knockout model is derived from the widely used Raji cell line and is validated to ensure absence of wild-type OSBPL2 protein expression, making it suitable for functional genomics, signaling studies, and drug screening.
The host cell line, Raji, originates from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma, representing a malignant B lymphocyte or lymphoblast. Raji cells are characterized by robust suspension growth, high transfection efficiency, and a well-defined role in B-cell biology, antibody production, and adaptive immunity. This cellular context provides a physiologically relevant platform to study lipid metabolism and oncogenic signaling in lymphoma. The EBV positivity adds another layer of relevance for studying viral interactions with host cell cholesterol homeostasis and immune evasion.
OSBPL2 encodes an oxysterol-binding protein-related protein that functions as a lipid transfer protein at endoplasmic reticulum?Cplasma membrane contact sites. It shuttles cholesterol between the two organelles by counter-exchanging with phosphatidylinositol-4-phosphate (PI4P), thereby modulating plasma membrane lipid raft composition. OSBPL2 is regulated by oxysterols such as 25-hydroxycholesterol and by SREBF2 in response to cellular sterol levels. It physically interacts with VAPA and VAPB at the ER surface and is functionally connected to the PI3K/AKT pathway: OSBPL2 acts upstream of AKT1 and mTOR, and its activity promotes expression of LDLR and HMGCR via SREBF2, thus influencing cholesterol homeostasis and AKT-mediated survival signals. Representative pathway components include OSBPL2, VAPA, OSBP, PI4KIII??, SAC1L, AKT1, and mTOR.
In the Raji B-cell lymphoma context, OSBPL2 knockout disrupts normal cholesterol trafficking, potentially altering lipid raft assembly and attenuating PI3K/AKT signaling, which is often hyperactivated in Burkitt lymphoma. This model enables dissection of OSBPL2-specific contributions to malignant B-cell growth, survival, and drug responsiveness, independent of other OSBP-related proteins. Given that OSBPL2 mutations have been linked to autosomal dominant nonsyndromic hearing loss and its expression changes in hepatocellular carcinoma and colorectal cancer, this knockout system provides a focused tool to explore lipid-dependent mechanisms in cancer biology, including the interplay between oxysterol signaling and immune cell function.
Researchers can employ OSBPL2 Knockout Raji Polyclonal Cells to investigate cholesterol metabolism in B-cell lymphoma, oxysterol-mediated signaling cascades, and PI3K/AKT pathway dynamics. They are well-suited for drug resistance studies, where altered lipid trafficking may affect sensitivity to chemotherapeutics or targeted agents, and for functional genomics screens involving OSBP-related proteins. Representative applications include western blotting for OSBPL2, RT-qPCR, quantitative cholesterol measurement, immunofluorescence for lipid droplets, flow cytometry for proliferation and apoptosis, phospho-AKT analysis, co-immunoprecipitation, and lipidomics. For further details, please contact Ascent Research.
