The LAMA5 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphoblast cell line. This product disrupts the LAMA5 gene, encoding laminin alpha-5, a subunit of laminin-511 and -521. The polyclonal pool provides a heterogeneous loss-of-function model for studying laminin-mediated processes in a B-cell lymphoma background without clonal selection artifacts.
Raji cells are an EBV-positive B lymphoblastoid line from a Burkitt lymphoma patient, widely used as a model for B-cell malignancies and immune response studies. They grow in suspension, express B-cell markers, and retain key signaling pathways relevant to lymphomagenesis, making them suitable for investigating tumor cell biology and viral oncogenesis.
LAMA5 encodes laminin ??5, which assembles with LAMB1 and LAMC1 to form laminin-511, a major basement membrane component. Through its LG domains, ??5 binds integrins ITGA3/ITGB1 and ITGA6/ITGB1, as well as dystroglycan (DAG1), to mediate adhesion and migration. Integrin engagement activates focal adhesion kinase (PTK2/FAK) and SRC, leading to AKT1 and MAPK1/3 (ERK) phosphorylation, thereby promoting survival and proliferation. LAMA5 expression is regulated by TGFB1, CTNNB1, and TP53. Knockout of LAMA5 ablates laminin-511/521, decoupling integrin signaling and impairing FAK, AKT, and ERK activation, thus disrupting ECM-receptor interaction and focal adhesion dynamics.
In Raji lymphoma cells, LAMA5 knockout disrupts adhesive interactions that govern tissue homing and transendothelial migration. This loss-of-function model enables dissection of how laminin-511-dependent adhesion influences lymphoma cell retention in protective niches, migratory behavior, and drug sensitivity. It offers a relevant system to explore the role of basement membrane components in B-cell malignancy hallmarks like anchorage-independent survival and metastatic dissemination.
These cells are suited for Western blotting, RT-qPCR, and immunofluorescence to validate LAMA5 loss, and functional assays such as adhesion and Transwell migration tests. Flow cytometry can assess integrin surface expression, while phospho-FAK and phospho-AKT analysis reveals signaling deficits. RNA-seq may uncover transcriptomic changes. Applications include studying integrin signaling in lymphoma, tumor microenvironment interactions, and drug resistance mechanisms. For further information, please contact Ascent Research.
