The FN1 Knockout Raji Polyclonal Cells represent a heterogeneous population of CRISPR/Cas9-edited Raji cells with targeted disruption of the FN1 gene. This polyclonal knockout cell product provides a versatile loss-of-function model for studying fibronectin biology in a human B lymphocyte background. The gene editing is achieved through CRISPR/Cas9-mediated genomic disruption, generating a mixed cell pool that reflects the diversity of editing outcomes across the population. As polyclonal knockout cells, this product is suitable for experiments where a consistent knockout phenotype at the population level is desired without single-cell cloning.
The host cell line, Raji, is a suspension-adapted lymphoblastoid cell line derived from a Burkitt’s lymphoma patient. Raji cells are Epstein-Barr virus (EBV)-positive and retain key characteristics of B lymphocytes, including immunoglobulin production and antigen presentation capabilities. These cells are widely used to model B cell biology, lymphomagenesis, and immune surveillance mechanisms. Their non-adherent growth properties and robust expansion in culture make them a practical system for functional genomics studies, particularly those investigating tumor microenvironment interactions and signaling pathways.
FN1 encodes fibronectin, a large extracellular matrix (ECM) glycoprotein that serves as a major structural component and mediates cell adhesion through integrin receptors, notably integrin ??5??1 and ??v??3. Fibronectin interacts with a variety of ECM and cell surface molecules, including collagen, fibrin, heparin, syndecan, and tenascin. Mechanistically, fibronectin-integrin engagement activates focal adhesion kinase (FAK) and Src family kinases, initiating downstream cascades such as the PI3K-Akt and ERK1/2 pathways. Upstream, FN1 expression is regulated by cytokines and transcription factors including TGF-??, TNF-??, NF-??B, and AP-1. Downstream, fibronectin-mediated signals modulate small GTPases (Rac1, RhoA) and cytoskeletal reorganization, influencing cell migration and survival. In Raji B cells, FN1 expression and the resulting autocrine or paracrine ECM signals may contribute to adhesion-dependent signaling that intersects with B cell receptor and survival pathways.
Disruption of FN1 in Raji cells is expected to compromise fibronectin deposition and integrin-mediated adhesion, thereby altering signaling events that depend on FAK, Src, and Akt activation. Given the role of fibronectin in cell migration and ECM remodeling, the FN1 knockout model enables investigation of how loss of this matrix protein affects B lymphocyte interaction with the microenvironment. In the context of lymphoma biology, FN1 knockout may influence tumor cell dissemination, drug resistance, and immune evasion. Additionally, the polyclonal nature of the population mimics the genetic heterogeneity observed in tumor cell populations, providing a more physiologically relevant system for certain functional assays.
This product is suited for a broad range of research applications, including the study of B cell adhesion and migration, tumor microenvironment interactions, and ECM remodeling in lymphoma. Representative assays that can be performed with these knockout cells include cell adhesion assays, Transwell migration assays, and phospho-signaling analysis to quantify alterations in integrin and growth factor signaling pathways. Additionally, Western blotting, RT-qPCR, and flow cytometry can validate FN1 knockout and assess changes in downstream targets such as FAK, ERK1/2, and Akt. Further functional studies may employ co-immunoprecipitation to examine protein-protein interactions or RNA-seq for transcriptome-wide analysis. For more information on this product or to discuss custom applications, please contact Ascent Research.
