The CCDC50 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes carrying a disrupted CCDC50 gene. This polyclonal knockout model enables loss-of-function studies without monoclonal selection, preserving diverse genetic backgrounds within the cell pool. Gene disruption was achieved using CRISPR/Cas9 technology, and the resulting polyclonal cells are suitable for investigating the functional consequences of CCDC50 ablation in a B-cell context.
The Raji cell line, derived from a Burkitt’s lymphoma patient, is an Epstein-Barr virus-positive human B lymphocyte model widely used in immunology and cancer research. Raji cells exhibit key features of adaptive immunity, including antigen presentation and antibody production, and serve as a relevant system for studying B-cell signaling, endocytosis, and viral oncogenesis.
CCDC50 encodes a multifunctional protein that negatively regulates epidermal growth factor receptor (EGFR) signaling by targeting activated EGFR for lysosomal degradation, thereby dampening downstream RAS-RAF-MEK-ERK pathway activity. Additionally, CCDC50 acts as an inhibitor of RIG-I-mediated antiviral innate immunity by disrupting the RIG-I (DDX58)?CMAVS interaction, which prevents TBK1-mediated phosphorylation of IRF3 and IRF7, ultimately reducing type I interferon production. Interacting partners include EGFR, RIG-I, MAVS, and ubiquitin ligases.
In the Raji B-lymphocyte background, which exhibits robust endocytic machinery and expresses EGFR, the loss of CCDC50 is predicted to enhance EGFR stability and sustained signaling, potentially impacting cell proliferation and survival. Concomitantly, ablation of CCDC50??s immune-regulatory function may unleash RIG-I-dependent antiviral responses, including upregulation of interferon-stimulated genes, making these cells a valuable tool for dissecting the crosstalk between growth factor and innate immune pathways.
These polyclonal knockout cells are designed for diverse research applications, including EGFR degradation kinetics assays via western blot, RIG-I signaling analysis using luciferase reporter systems, and co-immunoprecipitation to examine disrupted protein interactions. Additional assays such as flow cytometry for EGFR surface expression, RT-qPCR for interferon-stimulated gene quantification, and apoptosis profiling further expand experimental utility. Researchers can leverage this model to explore cancer biology, antiviral immunity, endocytic trafficking, and autophagy regulation. For more details, please contact Ascent Research.
