CXCR4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphoblastoid cell line, engineered to disrupt the CXCR4 gene. This loss-of-function model enables researchers to study CXCR4-dependent signaling and biological processes without the variability of single-cell clones. The polyclonal format preserves the heterogeneous genetic background of the parental Raji line, providing a robust tool for functional genomics studies.
The Raji cell line originates from EBV-positive Burkitt’s lymphoma, representing a well-established model for B-cell lymphoma and immune studies. These B lymphocytes exhibit lymphoblastoid morphology and are widely used in antibody production, immunology, and cancer research. The Raji line’s tumorigenic background and expression of key B-cell markers make it particularly suitable for investigating chemokine-mediated signaling in lymphoid malignancies.
CXCR4 encodes a G protein-coupled receptor that specifically binds the chemokine CXCL12. Upon ligand stimulation, CXCR4 activates G??i and G?¦? subunits, leading to downstream signaling through PI3K/AKT and MAPK/ERK pathways. Specifically, CXCL12?CCXCR4 engagement triggers PI3K-mediated AKT phosphorylation, promoting cell survival, while G?¦? activates PLC, elevating intracellular Ca2? and regulating cytoskeletal dynamics. ??-arrestin2 recruitment facilitates ERK1/2 activation and receptor internalization. CXCR4 expression is regulated by upstream factors including HIF-1??, TGF-??, EGF, and VEGF, and it interacts with co-receptors CD4 and CCR5, as well as caveolin-1 and filamin A. Downstream effects encompass transcriptional regulation via NF-??B, JNK, p38, and ??-catenin, and modulation of integrins and MMPs, thereby influencing migration, adhesion, and invasion. Representative signaling modules include CXCL12 ?? CXCR4 ?? G??i ?? PI3K ?? AKT and CXCL12 ?? CXCR4 ?? ??-arrestin ?? ERK.
In Raji cells, CXCR4 signaling contributes to lymphoma cell migration, proliferation, and survival. Disruption of CXCR4 in this B-cell lymphoma model allows dissection of chemokine-dependent pathways that govern tumor microenvironment interactions, immune cell trafficking, and lymphoma pathogenesis. Moreover, since Raji cells are susceptible to HIV infection via CD4 and CXCR4, this knockout model is valuable for studying HIV entry mechanisms and evaluating CXCR4-targeted antiviral or anti-cancer strategies.
These CXCR4 Knockout Raji Polyclonal Cells are suitable for a wide range of experimental approaches, including functional migration assays using transwell or microfluidic systems, phospho-signaling analysis by immunoblotting or flow cytometry, apoptosis and survival assays, and transcriptomic profiling via RNA-seq. Researchers can employ this model to validate CXCR4-targeted therapies, investigate chemokine-mediated immune cell recruitment, and explore crosstalk between CXCR4 and other oncogenic pathways in B-cell malignancies. For further technical details or to discuss your experimental needs, please contact Ascent Research.
