The CD164 Knockout Raji Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line, in which the CD164 gene has been disrupted to generate a loss-of-function model. The polyclonal format provides a genetically heterogeneous knockout pool, enabling studies that require a population-level assessment of CD164 function without clonal selection biases. This cellular model is designed for advanced biomedical research applications focused on cell adhesion, migration, and signaling pathways.
Raji cells are a well-characterized human B lymphocyte line originally established from an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma. These cells retain key B cell functions, including antibody production and antigen presentation, and are widely used in immunology and cancer research. The EBV-positive status and lymphomagenic origin make Raji a relevant model for studying B cell malignancies and virus-host interactions. The suspension growth characteristics and robust proliferative capacity of Raji cells facilitate scalable experimental workflows.
CD164 encodes a sialomucin adhesion receptor that plays critical roles in cell adhesion, migration, proliferation, and hematopoietic stem cell homing. Mechanistically, CD164 is activated by CXCL12 (SDF-1) and Notch ligands, and it functions upstream of cell cycle genes, integrins, and Rho GTPases. CD164 directly interacts with CXCR4, integrin ??4??1 (VLA-4), Notch1, L-selectin, and Ezrin. These interactions integrate CXCR4 signaling, integrin-mediated adhesion, and Notch signaling pathways to modulate cell motility and stem cell niche retention. Additionally, CD164 is implicated in the regulation of hematopoietic stem cell homing and tumor metastasis through these molecular networks.
In B lymphocytes, CD164-mediated adhesion and migration are relevant for lymphocyte trafficking, lymph node homing, and potentially for the dissemination of B cell lymphomas. Disruption of CD164 in Raji cells provides a platform to dissect the contribution of this sialomucin to B cell adhesion to vascular endothelium and extracellular matrix components, as well as to CXCL12/CXCR4 chemotactic responses. This model is particularly valuable for exploring the role of CD164 in B cell malignancies, including its potential involvement in the pathology of acute myeloid leukemia, multiple myeloma, and myelodysplastic syndromes, given the shared signaling axes.
The CD164 knockout Raji polyclonal cells support diverse functional assays, including flow cytometry and western blotting to verify CD164 deficiency and downstream signaling, transwell migration and adhesion assays to quantify chemotaxis and cell?Cmatrix interactions, co-immunoprecipitation to probe protein interactions, and in vivo homing assays to track biodistribution. Colony-forming unit assays may evaluate clonogenic potential in co-culture. This model enables research into hematopoietic stem cell biology, cancer metastasis, immunology, and drug discovery. For assistance, contact Ascent Research.
