The MSN Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the MSN gene. This product provides a heterogeneous pool of edited Raji cells, enabling the study of moesin function without clonal selection artifacts. As a polyclonal population, it mitigates clonal idiosyncrasies and is well-suited for bulk assays such as signaling studies, adhesion experiments, and drug screening. The knockout is achieved via CRISPR/Cas9-mediated gene disruption, creating a loss-of-function model for the membrane-cytoskeleton linker protein moesin.
The host cell line, Raji, is a human B lymphoblastoid cell line derived from a Burkitt lymphoma patient. Raji cells are Epstein-Barr virus (EBV)-positive and carry the characteristic t(8;14) chromosomal translocation that places the c-MYC oncogene under the immunoglobulin heavy chain enhancer, driving constitutive proliferation. Widely used as a model for B cell biology, immunology, and lymphoma research, these cells express mature B cell surface markers and can be stimulated to investigate B cell receptor signaling, antigen presentation, and tumor microenvironment interactions.
MSN encodes moesin, a member of the ezrin/radixin/moesin (ERM) family that crosslinks filamentous actin (F-actin) to the plasma membrane. Moesin is activated by ROCK-mediated phosphorylation at threonine 558, downstream of the small GTPase RhoA. Upon activation, moesin bridges F-actin to transmembrane receptors such as ICAM-1, ICAM-2, and CD44, and scaffolds with adaptor proteins like EBP50/NHERF1. It functionally interacts with ezrin and radixin, and its membrane association is enhanced by PIP2. Moesin integrates signals from chemokine receptors (e.g., CXCR4) and integrins, regulating cell shape, adhesion, migration, and B cell receptor signaling.
In Raji cells, MSN knockout elucidates moesin??s role in B cell adhesion, transendothelial migration, and immunological synapse organization??processes critical for lymphomagenesis. This model aids in dissecting how RhoA-ROCK-moesin signaling drives lymphoma progression and immune cell function, with implications for immunodeficiency, autoimmunity, and cancer metastasis. The EBV-positive background further allows investigation of viral-lymphoma interactions and their impact on cytoskeletal dynamics.
Typical applications include Western blotting for moesin and phospho-moesin to confirm protein loss, immunofluorescence for F-actin localization, flow cytometry for adhesion molecule expression, and cell migration/adhesion assays. Researchers can employ RhoA activation assays to probe upstream signaling or use the cells in high-content screens for compounds targeting the RhoA-ROCK-moesin pathway. This model supports studies of B cell activation, immunological synapse formation, and lymphomagenesis. For further information, please contact Ascent Research.
