The CGNL1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, designed to disrupt the expression of the CGNL1 gene (cingulin-like 1). This pooled knockout model provides a powerful loss-of-function system for investigating CGNL1-dependent mechanisms in a B-cell context, without the limitations of single-cell clonal selection. The polyclonal format offers a heterogeneous mixture of knockout alleles, enabling robust phenotypic studies while maintaining genetic diversity that more closely reflects population-level responses.
The Raji host cell line originates from a Burkitt’s lymphoma patient and is characterized by its Epstein-Barr virus (EBV)-positive status and mature B lymphocyte phenotype. Raji cells are widely employed in immunology and oncology research owing to their capacity for antigen presentation, robust proliferation, and well-defined signaling networks. This model cell line serves as a relevant platform for examining how junctional scaffold proteins, traditionally studied in epithelial tissues, influence lymphocyte functions such as adhesion, migration, and immune synapse formation.
CGNL1 encodes a scaffold protein localized to tight junctions and adherens junctions, where it interacts with key polarity regulators including PAR3, aPKC, and the actin cytoskeleton. It plays a critical role in maintaining epithelial barrier integrity by coupling Rho GTPase signaling to junctional complex assembly. Mechanistically, CGNL1 functions downstream of aPKC and Rho GTPases, and upstream of tight junction components such as ZO-1, claudins, and occludin. Additionally, CGNL1 associates with cingulin, JACOP, E-cadherin, and ??-catenin, thereby integrating cell-cell adhesion with actin organization. Its disruption destabilizes apical-basal polarity and increases paracellular permeability, highlighting its central role in cell polarity pathways.
In the Raji B lymphocyte background, this CGNL1 knockout model opens avenues to explore non-epithelial functions of a canonical junctional scaffold. Although CGNL1 is not typically expressed at high levels in hematopoietic cells, emerging evidence suggests that junctional proteins can influence lymphocyte migration, homing, and malignant transformation. Therefore, this polyclonal knockout product is particularly valuable for studying the contribution of CGNL1 to B cell lymphoma pathogenesis, cancer cell invasion, and immune cell polarity. It enables researchers to dissect how loss of CGNL1 affects actin cytoskeleton dynamics and signaling in a Burkitt’s lymphoma context.
This polyclonal product is ideally suited for a range of advanced applications, including functional genomics, drug target validation, and mechanistic studies of CGNL1 in non-adherent cells. Typical experimental workflows include Western blotting and RT-qPCR to confirm gene disruption, RNA-seq to assess transcriptomic alterations, flow cytometry for surface marker profiling, and co-immunoprecipitation to probe protein-protein interactions. Migration assays and phospho-signaling analyses can be employed to evaluate the impact on cell motility and downstream pathways. For further information or technical support, please contact Ascent Research.
