The FER Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, engineered to disrupt the FER gene. This heterogeneous pool enables loss-of-function studies in a defined B lymphocyte background, avoiding clonal selection biases and passage artifacts associated with monoclonal lines. The polyclonal format provides a more representative model of FER deficiency within tumor-derived B cells, allowing researchers to investigate FER-dependent signaling without clonal variation effects.
The Raji line is an EBV-positive Burkitt lymphoma B lymphoblastoid cell line widely used in immunological and cancer research. Derived from a Burkitt lymphoma patient, these cells display a B lymphocyte phenotype, lymphoblastoid features, and tumorigenicity in xenografts. Raji cells express key B cell markers and are permissive for studies of B cell receptor (BCR) signaling, Fc receptor-mediated functions, and lymphomagenesis. Their robust growth and well-characterized biology make them a reliable host for genetic perturbation studies of B cell malignancies.
FER encodes a non-receptor tyrosine kinase activated downstream of integrin receptors, cytokine receptors, BCR, and growth factors. It phosphorylates substrates such as p120 catenin, cortactin, and STAT3, thereby regulating adhesion, migration, and proliferation. In immune contexts, FER mediates integrin beta1-dependent adhesion and JAK-STAT signaling, connecting extracellular inputs to cytoskeletal and transcriptional outputs. Its interactions with integrins and adaptors position it at a node controlling B lymphocyte behavior and tumor progression.
In Raji cells, FER knockout is expected to impair integrin-dependent adhesion and migration, and attenuate STAT3 phosphorylation downstream of BCR and cytokine receptors. This disruption likely compromises the malignant phenotype of Burkitt lymphoma, affecting proliferation and survival. By ablating FER in tumorigenic B cells, the model allows dissection of FER’s role in lymphomagenesis and crosstalk with Fc receptor and JAK-STAT signaling. The EBV-positive background also permits study of viral latency intersections with FER signaling.
These cells are suitable for Western blotting of phospho-FER and substrates, flow cytometry for integrin expression and adhesion, and migration or proliferation assays. Co-immunoprecipitation can probe FER-p120 catenin/cortactin interactions, and the cells support drug target validation for FER-dependent pathways in B-cell lymphoma and leukemia. They also enable studies of inflammatory disorders involving FER. For further details or to discuss experimental design, please contact Ascent Research.
