EXOC4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with disruption of the EXOC4 gene. The polyclonal nature provides a robust loss-of-function model without single-cell cloning, preserving population diversity and reducing clonal artifacts. These cells are suitable for studying EXOC4-dependent processes in a B-cell lymphoma context, enabling investigation of exocyst complex function and vesicle trafficking pathways.
The parental Raji cell line is an EBV-positive Burkitt’s lymphoma-derived B lymphocyte model widely used in immunology and cancer research. Raji cells exhibit features of mature B cells, including surface immunoglobulin expression, antigen-presentation capabilities, and active secretory pathways. Their transformed phenotype and rapid proliferation make them a workhorse for studying B-cell receptor signaling, lymphomagenesis, and exocytosis. Because Raji cells endogenously express components of the exocyst complex, they provide a relevant physiological context for dissecting EXOC4 function in membrane trafficking and immunoglobulin secretion.
EXOC4 (Sec8) is a core subunit of the octameric exocyst complex, which orchestrates vesicle tethering to the plasma membrane prior to SNARE-mediated fusion. In Raji cells, EXOC4 is regulated by the small GTPases RalA and RalB, activated downstream of PI3K/AKT and mTOR signaling. The exocyst complex, comprising EXOC1?CEXOC8, interacts with SNARE proteins such as VAMP2, SNAP23, and Syntaxin4 to promote vesicle docking. EXOC4 knockout disrupts this assembly, impairing exocytosis and altering surface delivery of receptors and secreted immunoglobulins. Consequently, EXOC4 loss uncouples key membrane trafficking events downstream of Ral GTPases and CDC42, affecting cell polarity and secretion.
In the Raji B-lymphocyte model, EXOC4 deficiency severely impairs immunoglobulin secretion and disrupts surface receptor dynamics, compromising antigen presentation and B-cell signaling. The polyclonal EXOC4 knockout population thus serves as a powerful tool to dissect polarized exocytosis in lymphocyte biology and to identify molecular vulnerabilities in B-cell malignancies. Researchers can examine how exocyst dysfunction influences cell migration, focal adhesion turnover, and crosstalk with the tumor microenvironment, all implicated in lymphoma metastasis.
Typical applications include Western blotting and immunofluorescence to assess EXOC4 depletion and exocyst localization, ELISA to quantify immunoglobulin secretion defects, flow cytometry to measure surface receptor levels, and migration assays to evaluate metastatic potential. Co-immunoprecipitation experiments can probe exocyst assembly integrity, while pHluorin-based vesicle trafficking assays directly visualize secretion dynamics. This product is valuable for validating EXOC4 as a therapeutic target and for screening modulators of exocytosis. For further information, please contact Ascent Research.
