The DLG5 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated through targeted disruption of the DLG5 gene in the human Raji B lymphocyte host cell line. This polyclonal product preserves genetic heterogeneity inherent to a population-level knockout, offering a versatile loss-of-function model for bulk functional studies without artifacts from single-cell cloning. By abolishing DLG5 protein expression across a pool of edited cells, researchers gain a tool to interrogate scaffold-mediated signaling in a well-characterized lymphoblastoid system.
The Raji cell line originates from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma patient, establishing it as a foundational model in immunology and lymphoma research. These suspension-adapted B lymphocytes exhibit robust proliferation, high transfection efficiency, and stable maintenance in culture, enabling efficient CRISPR/Cas9 gene editing and consistent experimental outcomes. Their EBV association drives oncogenic pathways that intersect with cell polarity and adhesion signaling, providing a physiologically relevant context for studying DLG5 function.
DLG5 encodes a membrane-associated guanylate kinase (MAGUK) scaffold protein that coordinates cell adhesion with intracellular signaling networks. It directly interacts with angiomotin (AMOT) and YAP to modulate Hippo pathway activity, controlling YAP/TAZ nuclear translocation and transcriptional regulation of downstream targets such as CTGF and CYR61. Concurrently, DLG5 engages with cadherins and ??-catenin at tight junctions, linking Wnt signaling to junctional complex assembly. Upstream regulators including MST1/2 and LATS1/2 kinases, as well as Wnt ligands, converge on DLG5 to fine-tune tight junction integrity and cell proliferation, positioning it as a critical node in epithelial polarity and cancer pathways.
Disruption of DLG5 in Raji B lymphocytes creates a distinctive platform for exploring non-epithelial roles of this scaffold protein, particularly in hematological malignancy. The knockout enables dissection of Hippo and Wnt crosstalk in a lymphoma background, where angiomotin/YAP complexes may drive aberrant proliferation. Phenotypic consequences??such as altered cell adhesion, migration, or survival??can be directly attributed to DLG5 loss, offering insights into Burkitt lymphoma progression and potential therapeutic vulnerabilities. This model bridges epithelial cell biology with immune cell contexts, expanding the utility of DLG5 research beyond traditional barrier function studies.
Experimental applications for these polyclonal knockout cells are broad and include quantitative analysis of YAP/TAZ activity by flow cytometry, Western blotting for pathway components, and RT-qPCR profiling of target genes like CTGF. Functional assays such as cell proliferation, migration, and xenograft tumor growth provide robust readouts for lymphoma behavior, while co-immunoprecipitation and immunofluorescence can validate DLG5 protein interactions and tight junction protein localization. The polyclonal format is especially suited for drug screening campaigns testing Wnt/Hippo modulators, as it mirrors heterogeneous tumor cell populations. For further technical details or assistance, please contact Ascent Research.
