The DOCK7 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt lymphoma Raji B lymphocyte line, featuring targeted disruption of the DOCK7 gene. This polyclonal pool enables loss-of-function analysis of DOCK7 in an EBV-positive B cell background, circumventing the clonal selection artifacts often associated with single-cell-derived knockout models. The product is supplied as a viable polyclonal population and is suitable for a wide range of cellular and molecular assays.
The Raji host cell line is a suspension-adapted human B lymphocyte line originally isolated from a Burkitt lymphoma patient. These cells harbor Epstein-Barr virus (EBV) and express characteristic B cell surface markers, making them a widely used model in immunology, virology, and oncology research. Raji cells exhibit robust proliferation and are amenable to genetic manipulation, enabling investigations into B cell receptor signaling, apoptosis, and lymphomagenesis. Their EBV-positive status also provides a unique platform to study virus-host interactions and their impact on B cell biology.
DOCK7 functions as a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPases Rac1 and Cdc42 by catalyzing the exchange of GDP for GTP. In signal transduction, DOCK7 operates downstream of receptor tyrosine kinases, integrin engagement, and PI3K-mediated signaling. It forms a functional complex with the adaptor protein ELMO1, facilitating localized GTPase activation at the plasma membrane. Once activated, Rac1 and Cdc42 orchestrate a cascade that includes PAK kinases, the WAVE regulatory complex, LIM kinase, cofilin, and Arp2/3-mediated actin nucleation, ultimately driving dynamic reorganization of the actin cytoskeleton. This signaling module is essential for cell migration, adhesion, neuronal morphology, and axon guidance, and is implicated in adherens junction stability. DOCK7 also interacts with TACC3, suggesting additional roles in microtubule dynamics.
In Raji B lymphocytes, DOCK7-mediated cytoskeletal dynamics are expected to underpin migration, adhesion, and immunological synapse formation. The EBV-positive background of these cells offers an opportunity to study how DOCK7 contributes to viral persistence and B cell transformation. Since aberrant activation of Rac1/Cdc42 is frequently observed in lymphomas, this knockout model can help clarify the role of DOCK7 in lymphomagenesis and immune cell function. While DOCK7 mutations are primarily associated with neurodevelopmental disorders, its function in non-neuronal lineages underscores the broader relevance of actin regulatory networks in disease states.
This polyclonal knockout product enables functional studies using transwell migration assays, adhesion assays, and immunofluorescence for actin visualization. Rac1/Cdc42 activation can be measured by G-LISA, while downstream signaling is assessable via phospho-PAK western blotting. Additional applications include flow cytometry, proliferation assays, and transcriptome analysis by RNA-seq. Collectively, these approaches facilitate dissection of DOCK7-dependent pathways in B cell biology and lymphoma research. For further information, please contact Ascent Research.
