PARD6B Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Burkitt lymphoma Raji cell line. These cells harbor targeted disruption of the PARD6B gene, enabling robust loss-of-function analysis within a B lymphoblastoid context. The polyclonal format preserves allelic heterogeneity, making it well-suited for functional assays that require population-wide phenotypes without clonal bias.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. It expresses canonical B cell surface markers and is widely employed as a model for B cell lymphoma and EBV-mediated oncogenesis. Raji cells grow in suspension, exhibit rapid proliferation, and retain key B cell receptor and chemokine signaling pathways, offering a physiologically relevant system for studying lymphocyte polarity and migration.
PARD6B encodes a scaffold protein of the Partitioning-Defective (PAR) polarity complex. It couples activated CDC42 GTPase to atypical protein kinase C (aPKC), which phosphorylates substrates including PARD3 (Par3), Lethal giant larvae (Lgl), and MARCKS. This pathway establishes apical-basal polarity in epithelia and regulates front-rear polarity in migrating lymphocytes. In immune cells, PARD6B operates downstream of chemokine receptors, promoting Rac1 activation via TIAM1 and subsequent actin cytoskeleton remodeling. Upstream regulators include TGFBR2 and SMURF1, while Rho GTPases integrate broader cytoskeletal cues. Interacting partners Par3, aPKC, and TIAM1 form the core complex, and downstream effectors such as ZO-1 and occludin mediate tight junction formation in polarized cells.
This knockout model provides a relevant tool for investigating PARD6B-dependent polarity and migration in malignant B cells. The EBV-positive Raji background allows dissection of viral?Chost interactions that may alter polarity to promote lymphomagenesis. By ablating PARD6B function, researchers can examine its role in B cell activation, immune synapse organization, chemotaxis, and potential drug resistance mechanisms.
Researchers can leverage these cells for transwell migration assays, immunofluorescence microscopy of actin and tight junction proteins, flow cytometric assessment of polarity markers, and co-immunoprecipitation of the PAR complex. Phospho-aPKC and Rac1 signaling analyses, western blotting for PARD6B verification, and drug sensitivity screens are also applicable. These knockout cells support studies on lymphocyte polarity, immune synapse dynamics, and lymphoma biology. For further information, please contact Ascent Research.
