The EGFR Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes carrying disruption of the epidermal growth factor receptor (EGFR) gene. This knockout model provides a polyclonal loss-of-function system, avoiding confounding effects from monoclonal selection while enabling robust analysis of EGFR-dependent signaling and cellular responses in a lymphoid background. The polyclonal nature ensures representation of diverse editing events, making it suitable for population-level studies of EGFR function.
The Raji host cell line is a well-characterized human B lymphocyte line derived from an EBV-positive Burkitt lymphoma, widely used to model humoral immunity, antibody production, and B cell malignancies. Raji cells retain key features of activated B cells, including expression of surface immunoglobulins and various cytokine receptors, and provide a relevant cellular context for investigating oncogenic signaling pathways that drive lymphomagenesis. The EBV status further allows interrogation of viral?Chost interactions that may intersect with receptor tyrosine kinase signaling.
EGFR encodes a receptor tyrosine kinase activated by ligands including EGF, TGF-alpha, HB-EGF, amphiregulin, epiregulin, and betacellulin. Ligand-induced dimerization triggers autophosphorylation and initiates the MAPK/ERK cascade (EGFR ?? GRB2 ?? SOS ?? RAS ?? RAF ?? MEK ?? ERK), leading to activation of transcription factors FOS, JUN, and MYC; the PI3K/AKT pathway with AKT1 and negative regulator PTEN; and the JAK/STAT pathway involving STAT3. Adaptor proteins GRB2, SOS1, SHC1, GAB1, and the E3 ligase CBL assemble proximal signaling complexes. These pathways drive proliferation, survival, and migration.
In Raji B lymphocytes, EGFR signaling contributes to proliferative and survival programs, and its dysregulation may cooperate with EBV-driven oncogenic events in lymphomagenesis. EGFR knockout abolishes ligand-dependent receptor activation, disrupting downstream MAPK/ERK and PI3K/AKT cascades and impairing proliferative and survival responses. This polyclonal knockout cell model allows direct assessment of EGFR dependency in B cell malignancies and exploration of EGFR-mediated modulation of immune cell functions such as antibody production and cytokine responsiveness. By uncoupling EGFR from its effectors, the model clarifies the receptor??s specific contribution in a B lymphocyte background.
Typical applications include studying EGFR signaling in B cell malignancies, therapeutic target validation, drug sensitivity screening, and immune cell function analysis. Compatible assays encompass western blotting for EGFR and phospho-ERK, flow cytometry for surface EGFR, proliferation assays (MTS/MTT), apoptosis assays (Annexin V), RT-qPCR for FOS and MYC, and phospho-signaling profiling. These tools support preclinical oncology and immunology research. For additional information, please contact Ascent Research.
