The LGALS3BP Knockout Raji Polyclonal Cells comprise a polyclonal population of Raji B lymphocytes engineered via CRISPR/Cas9-mediated disruption of the LGALS3BP gene, encoding the secreted glycoprotein galectin-3-binding protein (Mac-2BP/90K). This pooled knockout model offers a heterogeneous loss-of-function system that preserves population-level variability, avoiding the selection bias of clonal isolates and enabling robust assessment of LGALS3BP function in a physiologically relevant, mixed genetic background suitable for downstream bulk assays.
Raji is an EBV-positive human Burkitt lymphoma B cell line derived from a patient, expressing hallmark B cell surface antigens CD19, CD20, CD22, and CD79a. It serves as a standard model for studying EBV-associated B cell lymphomagenesis, antigen presentation, and BCR signaling. Constitutive activation of NF-??B and PI3K/AKT pathways in Raji underscores its utility in dissecting molecular mechanisms of B cell malignancies and viral oncogenesis.
LGALS3BP encodes a heavily glycosylated, multidomain secreted scaffold that interacts with galectin-1, galectin-3, integrin ??1 (ITGB1), collagens, fibronectin, and CD33 to modulate cell adhesion, aggregation, and signaling. Upstream, transcription is activated by IFN-??, IFN-??, and TNF-??. Downstream, LGALS3BP drives NF-??B signaling through RELA and NFKB1, enhances STAT3 activity, stimulates AKT1 phosphorylation, and promotes the expression of pro-inflammatory mediators IL-6, IL-8, and MMP-9. Knockout in Raji cells is therefore anticipated to dampen these pathways, reducing cytokine secretion and adhesion-dependent signaling.
In the Raji lymphoma context, loss of LGALS3BP is predicted to compromise NF-??B and STAT3 transcriptional programs that sustain proliferation, survival, and immune evasion. Additionally, because LGALS3BP is secreted, its absence may alter tumor?Cstroma crosstalk by perturbing galectin?Cmatrix interactions, potentially impacting lymphoma progression. This polyclonal knockout model thus provides a relevant system to dissect LGALS3BP’s contribution to B cell lymphoma biology and EBV-mediated immune modulation.
Researchers may utilize these cells for Western blotting and RT-qPCR to verify gene disruption, flow cytometry for B cell marker expression, NF-??B luciferase reporter assays, cytokine ELISA (IL-6, IL-8), cell adhesion assays, proliferation measurements via MTS or CFSE dilution, and transcriptomic analysis by RNA-seq. Such assays support investigations of LGALS3BP function in B cell lymphoma, tumor microenvironment dynamics, drug target validation, and cytokine regulation, bridging basic and translational research. For further technical details, please contact Ascent Research.
