The MEMO1 Knockout Raji Polyclonal Cells consist of a mixed population of Raji cells carrying CRISPR/Cas9-mediated disruptions in the MEMO1 gene. This polyclonal knockout model originates from targeted genetic editing that introduces loss-of-function variants across the bulk culture, providing a heterogeneous yet gene-deficient cellular background. The product is provided as live cells ready for expansion and downstream experimental application.
The Raji parental line is a human Burkitt’s lymphoma-derived B lymphocyte model, noted for its antibody production and antigen presentation capabilities. These cells proliferate rapidly, display mature B cell surface markers, and are extensively utilized in immunological and cancer research. Their lymphoid context offers a relevant system to examine signaling pathways controlling B cell survival, adhesion, and migration.
MEMO1 encodes a scaffold protein that bridges activated receptor tyrosine kinases, notably ERBB2 and MET, to intracellular adaptors GRB2, SOS1, and SHC1. Ligand binding by EGF or HGF triggers MEMO1-dependent assembly of signaling complexes that activate the MAPK/ERK cascade through HRAS, RAF1, MAP2K1, and MAPK1, and the PI3K/AKT pathway via PIK3CA and AKT1. These pathways converge on the small GTPases RAC1 and CDC42 to orchestrate actin cytoskeleton dynamics, thereby driving cell migration and invasion.
In the Raji Burkitt’s lymphoma background, MEMO1 knockout is expected to sever critical mitogenic and motility signals downstream of ERBB2 and MET, and potentially other RTKs. Given the dependence of Raji cells on tonic BCR and integrin signaling for viability and trafficking, loss of MEMO1 may attenuate both basal and ligand-stimulated phosphorylation of ERK1/2 and AKT1. This model thus enables dissection of MEMO1-dependent contributions to lymphoma cell motility, chemotaxis, and apoptotic resistance, illuminating mechanisms of disease progression.
These polyclonal knockout cells are amenable to diverse functional assays: Western blot analysis of phospho-ERK and phospho-AKT to gauge signaling output; Transwell migration and Matrigel invasion assays; immunofluorescence for F-actin to visualize cytoskeletal changes; flow cytometry to assess surface receptor abundance; and co-immunoprecipitation to characterize protein interaction networks. They serve as a powerful tool for validating RTK oncogenic targets, dissecting metastatic signaling modules in lymphoma, and screening chemical libraries for inhibitors of the MAPK/ERK or PI3K/AKT pathways. For further technical information, please contact Ascent Research.
