LAMB1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout population in the Raji B lymphoblastoid cell line, designed to disrupt expression of the LAMB1 gene. This loss-of-function model enables investigation of laminin ??1 subunit function in a B lymphocyte context. The polyclonal format provides a heterogeneous pool of edited cells, suitable for studying gene disruption effects without clonal isolation.
The Raji cell line, derived from a Burkitt lymphoma, is an Epstein?CBarr virus (EBV)-positive lymphoblastoid cell line widely used as a model for B cell biology, antigen presentation, and antibody production. These suspension-adapted cells maintain key characteristics of mature B lymphocytes and serve as a robust platform for functional genomics studies. Their lymphoblastoid origin makes them particularly relevant for exploring signaling networks and adhesion mechanisms governing B cell behavior.
LAMB1 encodes the laminin ??1 subunit, a critical component of laminin-111 (??1??1??1) and other heterotrimeric basement membrane glycoproteins. Through interactions with integrin receptors such as ??6??1 and ??3??1, dystroglycan, and nidogen, LAMB1 mediates cell adhesion, migration, and matrix assembly. Expression of LAMB1 is regulated by growth factors including TGFB1, EGF, HGF, and FGF2, and transcription factors AP-1 and STAT3. Downstream, laminin engagement activates focal adhesion kinase (FAK) and SRC, leading to phosphorylation of AKT and MAPK1/3, and ultimately influencing cytoskeletal reorganization via RAC1 and RHOA. Thus, LAMB1 integrates extracellular signals to control PI3K/Akt and MAPK/ERK pathways, as well as focal adhesion dynamics.
In the context of Raji B cells, LAMB1 knockout disrupts integrin-mediated adhesion and signaling, potentially impairing cell migration and lymphocyte homing. Given the role of laminins in lymphoid tissue organization and immune cell trafficking, this model provides a tool to dissect how B cells interact with basement membranes and extracellular matrix. Disruption of LAMB1 may alter the ability of these lymphoma-derived cells to invade tissues, offering insights into cancer metastasis and the mechanisms underlying ECM remodeling in lymphomagenesis. Moreover, the model can be used to study the contribution of laminin?Cintegrin interactions to B cell activation and differentiation.
This polyclonal knockout cell population is suitable for a range of research applications, including the study of B cell migration and adhesion, basement membrane biology, and lymphocyte homing. It enables investigation of drug targeting of integrin?Claminin interactions and ECM remodeling in lymphoma. Typical assays include western blotting for LAMB1, RT-qPCR, flow cytometry for integrin expression, cell adhesion and migration assays, immunofluorescence for laminin organization, phospho-signaling analysis of FAK and AKT, and co-immunoprecipitation of laminin complexes. For additional technical details, please contact Ascent Research.
