This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte line, targeting the LLGL1 gene. The polyclonal configuration yields a mixed population of cells with disrupted LLGL1, avoiding clonal bias and providing a versatile loss-of-function model for studying tumor suppressor and polarity mechanisms.
Raji is an EBV-positive Burkitt’s lymphoma suspension cell line widely used in B cell immunology and oncology. Its rapid growth and well-documented signaling networks make it well-suited for investigating lymphomagenesis and tumor suppressors. The EBV-transformed background adds relevance to polarity and Hippo pathway studies, as viral proteins may intersect with these tumor-suppressive axes.
LLGL1 encodes a polarity scaffold protein that functions as a tumor suppressor and regulator of asymmetric division. It associates with the Par complex, being phosphorylated by aPKC in conjunction with Par6, and scaffolds interactions with SCRIB and DLG1 to control cytoskeletal dynamics through myosin II. Within Hippo signaling, LLGL1 acts upstream of MST and LATS kinases, thereby restricting YAP/TAZ co-activator activity. Its loss leads to YAP/TAZ derepression, and it also modulates Notch and Wnt pathways via Numb localization. LLGL1-dependent regulation of the actin cytoskeleton influences cell migration and adhesion, further tying polarity to metastatic potential. These intermolecular connections underscore LLGL1’s role at a signaling nexus controlling proliferation and apoptosis.
In Raji B cells, LLGL1 depletion disrupts cell polarity and Hippo control, potentially driving oncogenic features including enhanced proliferation and survival. The loss of asymmetric division may shift cell fate toward self-renewal, cooperating with EBV-mediated transformation. This model allows assessment of altered YAP/TAZ target expression, cytoskeletal defects, and signaling cross-talk in a lymphoma-relevant context. Additionally, the polyclonal nature permits evaluation of population-level responses and heterogeneous knockout effects, simulating a more physiologically relevant loss of LLGL1.
Typical applications include cell polarity and Hippo signaling studies in lymphocytes, using assays such as proliferation, apoptosis, migration, Western blotting, and immunofluorescence to monitor YAP, TAZ, aPKC, and SCRIB. Drug sensitivity screening can identify compounds targeting LLGL1-deficient lymphomas. The model also suits asymmetric division and tumor suppression research in B cells. For further technical details or bulk pricing, please contact Ascent Research.
