The LLGL2 Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population in which the LLGL2 gene has been disrupted, providing a versatile loss-of-function model for investigating cell polarity and growth regulation in a B-cell context. As a polyclonal population, this product maintains genetic diversity while ensuring target-gene inactivation, enabling studies that more closely reflect the heterogeneity of tumor cells. The cells are generated using CRISPR/Cas9-mediated gene disruption and are supplied as a ready-to-use mixture of edited cells.
The host Raji cell line is a human B lymphoblastoid line derived from an Epstein?CBarr virus-positive Burkitt??s lymphoma. These cells are widely adopted in immunology and cancer research due to their origin in the B-cell lineage and their capacity for antibody production. Raji cells serve as a robust model for studying B-cell malignancies, adaptive immunity, and signaling pathways underlying lymphoma, making them an ideal platform for genetic perturbation studies.
LLGL2 is a core component of the Scribble polarity complex that governs apical?Cbasal polarity and suppresses cell proliferation through activation of the Hippo pathway. The protein interacts directly with DLG1 and SCRIB, and is regulated by the upstream polarity determinants aPKC, PAR3, PAR6, and the small GTPase Cdc42. LLGL2 also associates with non-muscle myosin heavy chains MYH9 and MYH10, linking polarity to actomyosin dynamics. In the absence of LLGL2, the Hippo kinase cascade (MST1/2 and LATS1/2) fails to phosphorylate and retain the transcriptional co-activators YAP and TAZ in the cytoplasm, resulting in their nuclear translocation and activation of pro-proliferative gene expression programs. This mechanistic connection places LLGL2 at the intersection of cell polarity, mechanical signaling, and growth control.
Within the Raji B-cell lymphoma background, LLGL2 knockout offers a physiologically relevant system to examine how disruption of polarity complexes contributes to lymphomagenesis. The interplay between polarity scaffolds and the Hippo/Wnt signaling networks is frequently altered in B-cell malignancies, and this model permits dissection of pathway crosstalk that may drive unchecked proliferation. It provides a unique tool for exploring the role of cell asymmetry in immune cell function and for identifying vulnerabilities that arise from polarity protein loss in lymphoma cells.
This LLGL2 knockout polyclonal cell population is suitable for a broad spectrum of biomedical research applications, including cancer cell biology, polarity complex investigation, and lymphoma pathogenesis. Experimentally, it supports Western blot analysis of LLGL2, YAP/TAZ, and phospho-MST/LATS; immunofluorescence staining for polarity markers; cell proliferation and migration/invasion assays; flow cytometric cell cycle analysis; and transcriptomic profiling via RNA-seq. The model also supports anti-cancer drug screening aimed at restoring Hippo pathway activity. For further information, please contact Ascent Research.
