EPB41 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by transient expression of Cas9 and guide RNAs targeting EPB41 in the Raji B-lymphocyte cell line. This polyclonal pool carries heterogeneous loss-of-function mutations at the EPB41 locus, enabling pooled functional studies without selection for single-cell clones. The product is supplied as proliferating suspension cells suitable for direct expansion and experimental use.
Raji cells are a well-characterized human B-lymphoblastoid cell line originally derived from an EBV-positive Burkitt lymphoma. They grow in suspension and are widely employed as a model for B-cell malignancies, Epstein?CBarr virus biology, and signaling pathways relevant to lymphomagenesis. Their transformed phenotype and ease of genetic manipulation make them a convenient platform for investigating genes involved in hematopoietic cell structure and function.
EPB41 encodes protein 4.1R, a spectrin-actin binding scaffolding protein that bridges transmembrane proteins to the cortical actin cytoskeleton, thereby regulating membrane stability, cell shape, and adhesion. 4.1R functions downstream of mechanical stimuli and upstream regulators such as GATA1 and TGF-??; it interacts with spectrin (SPTA1/SPTB), actin (ACTB), band 3 (SLC4A1), glycophorin C (GYPC), CD44, ezrin (EZR), and membrane palmitoylated protein 1 (MPP1). Through these interactions, EPB41 integrates cytoskeletal organization with Rho GTPase signaling, tight junction formation, and epithelial cell polarity pathways. Its scaffolding activity also influences downstream effectors including NUMA1 and PRKCA.
In Raji cells, disruption of EPB41 is expected to uncouple the plasma membrane from the underlying spectrin-actin network, potentially altering the rounded morphology typical of lymphocytes and impairing adhesion and migration capabilities. Given the role of 4.1R in B-cell receptor signaling and the EBV-transformed background, this knockout model offers a unique tool to dissect cytoskeletal contributions to lymphoma cell behavior, survival, and response to therapeutic agents.
Researchers can utilize EPB41 Knockout Raji Polyclonal Cells to investigate EPB41-dependent signaling networks via co-immunoprecipitation and proteomic profiling of the 4.1R interactome, to assess changes in actin organization by immunofluorescence, and to quantify adhesion (CD44) and migration defects using flow cytometry and transwell assays. The model is also suited for drug screening campaigns targeting cytoskeletal modulators in B-cell lymphomas and for RNA-seq studies to define transcriptomic alterations upon EPB41 loss. For further information, please contact Ascent Research.
