The EPB41L2 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human EPB41L2 gene in the Raji B lymphocyte line. This polyclonal format preserves the spectrum of editing outcomes across the cell pool, offering a robust loss-of-function model for investigating EPB41L2-dependent processes. The genomic disruption of EPB41L2 impairs expression of the encoded protein, erythrocyte membrane protein band 4.1-like 2, enabling functional dissection of its roles.
The Raji cell line, isolated from a Burkitt??s lymphoma patient, is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line extensively utilized in immunology and oncology. These cells retain key B cell features including surface immunoglobulin expression and antigen-presentation capacity, making them a pertinent model for humoral immunity and lymphomagenesis studies. Their transformed phenotype provides a relevant background for examining cytoskeletal and signaling perturbations central to B cell malignancies.
EPB41L2 encodes a member of the protein 4.1 family that functions as a scaffolding adapter linking transmembrane proteins to the spectrin-actin cytoskeleton. It directly interacts with NF2/Merlin, CD44, and the Par3/Par6 polarity complex, forming a molecular bridge between the plasma membrane and actin filaments. Downstream of cell adhesion receptors and Rho GTPase signaling, EPB41L2 modulates the Hippo pathway by recruiting NF2 and LATS1/2 kinases, which subsequently phosphorylate and inhibit YAP/TAZ transcriptional co-activators. Thus, EPB41L2 integrates mechanotransduction and polarity signals to control gene programs governing proliferation and apoptosis.
In Raji cells, disruption of EPB41L2 is predicted to compromise actin cytoskeleton integrity and tight junction formation, thereby altering cell adhesion and polarity. This impairment likely disrupts NF2/Merlin-mediated activation of LATS1/2, reducing YAP/TAZ phosphorylation and promoting their nuclear accumulation and oncogenic transcriptional activity. Consequently, the polyclonal knockout population serves as a physiologically relevant platform to dissect EPB41L2??s contributions to tumor suppression or progression in B cell lymphoma, particularly within Hippo pathway dysregulation.
These EPB41L2 knockout Raji cells enable a variety of functional assays, including immunofluorescence to visualize cytoskeletal reorganization, Transwell migration assays to assess chemotaxis, and drug sensitivity profiling via MTT assays. Phospho-YAP analysis and RNA-sequencing can delineate Hippo pathway status and global transcriptomic changes. The polyclonal knockout population is well-suited for high-throughput compound screens, co-culture experiments with stromal elements, and target validation studies in B cell lymphoma. For additional technical information, please contact Ascent Research.
