The LAMB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte cell line, featuring targeted disruption of the LAMB2 gene. The polyclonal format provides a heterogeneous pool of edited cells, enabling population-level functional analysis without clonal artifacts. This loss-of-function model is intended for studies of laminin ??2-dependent processes in B cell biology and extracellular matrix signaling.
Raji cells are an Epstein-Barr virus-positive Burkitt lymphoma-derived B lymphocyte line, widely used as a model for B cell malignancies and humoral immunity. Originating from an African Burkitt lymphoma, these suspension-adapted cells retain surface immunoglobulin expression and antigen-presenting capabilities, offering a well-characterized genetic background for gene-editing studies. Their robust growth and transformed phenotype make them particularly suitable for investigating tumor cell adhesion, migration, and drug resistance mechanisms.
LAMB2 encodes the laminin ??2 subunit, which assembles with laminin-?? and -?? chains to form heterotrimers such as laminin-??3??2??1 and -??6??2??1. These ECM proteins bind integrin receptors ??3??1, ??6??1, and ??7??1, as well as dystroglycan, and interact with nidogen and perlecan within basement membranes. Ligand engagement activates focal adhesion kinase (FAK) and SRC, initiating PI3K-AKT and ERK1/2 signaling cascades that regulate adhesion, migration, and survival. LAMB2 expression is transcriptionally controlled by TGF-??/SMAD, GATA, NF-??B, and AP-1 pathways, and is responsive to cytokines IL-1?? and TNF-??. Therefore, LAMB2 disruption severs this integrin-laminin signaling axis, potentially impairing FAK phosphorylation, AKT activation, and downstream cytoskeletal reorganization.
In Raji B cells, LAMB2 knockout offers a system to dissect laminin-integrin contributions to lymphoma cell behavior. Although suspension-adapted, Raji cells can adhere to ECM substrates via integrins, a process likely important for tumor microenvironment colonization and drug resistance. Loss of LAMB2 may attenuate adhesion to laminin-rich matrices, modulating migration and survival signals. This model thus facilitates investigation of ECM-integrin crosstalk in B-cell malignancies and provides insights into core laminin biology relevant to Pierson syndrome, congenital nephrotic syndrome, and muscle disorders.
Applications include Western blotting, RT-qPCR, and immunofluorescence to validate LAMB2 knockout, flow cytometry for integrin surface profiling, cell adhesion assays on ECM-coated surfaces, transwell migration studies, and phospho-FAK/phospho-AKT analysis. These polyclonal knockout cells are well-suited for pooled functional screens, tumor microenvironment interaction models, and drug resistance studies. For further information, please contact Ascent Research.
