The NAV2 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human Raji B lymphocyte line. This product features targeted disruption of the NAV2 gene, yielding a heterogeneous pool of loss-of-function models without clonal selection. The polyclonal format provides a robust population-based approach for studying NAV2-dependent processes, minimizing clonal artifacts and enabling experiments that reflect the genetic diversity inherent to knockout cell pools. Researchers can employ these cells to investigate how NAV2 loss affects cytoskeletal dynamics, cell migration, and signal transduction in a well-characterized B-cell background.
The Raji host cell line, derived from an EBV-positive Burkitt lymphoma, expresses B-cell markers CD19 and CD20 and grows in suspension. Widely used for EBV biology and B-cell malignancy studies, its EBV-positive status and latent gene expression make it relevant for viral-host interactions intersecting with NAV2 pathways. Its transformed phenotype and migratory capacity allow investigation of how NAV2 knockout alters lymphoma cell behavior.
NAV2 (Neuron Navigator 2) is a cytoskeletal adaptor bridging non-canonical Wnt signaling to actin and microtubule reorganization. Activated downstream of Wnt5a and Frizzled receptors, it interacts directly with Dishevelled (DVL) and plus-end tracking proteins EB1 and CLIP-170. NAV2 regulates Rho GTPases Rac1 and Cdc42, which control effectors PAK, LIMK, and cofilin to modulate Arp2/3-driven actin polymerization. It also associates with filamin A, linking signaling complexes to the actin cytoskeleton. This positions NAV2 at a critical node translating extracellular cues into polarized cytoskeletal responses, impacting morphology, adhesion, and directed movement.
In the Raji B-cell context, knockout of NAV2 is predicted to impair the cytoskeletal machinery required for cell migration and potentially for lymphoma cell dissemination. Given that EBV latent proteins like LMP1 can influence host cell signaling networks, NAV2 disruption may alter how these cells respond to microenvironmental cues, affecting their motility and invasive properties. The model thus enables dissection of NAV2’s role in the planar cell polarity pathway within a hematopoietic malignancy setting, offering insights into mechanisms that drive B-cell lymphoma progression and metastasis. Loss of NAV2 may also impact proliferation and survival pathways, making it a versatile tool for functional genomic studies.
These polyclonal knockout cells support Transwell migration assays, immunofluorescence of actin and microtubules, and Western blotting for NAV2 validation. Co-immunoprecipitation maps altered protein networks, Rho GTPase assays quantify Rac1/Cdc42 activity, and RNA-seq provides transcriptomic profiling. The model suits drug target validation for motility inhibitors and pathway dissection in B-cell malignancies. For further information, contact Ascent Research.
