EMD Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population disrupting the EMD gene, which encodes the nuclear envelope protein emerin. This suspension-adapted B lymphocyte model provides a consistent loss-of-function background for population-level studies. The polyclonal format maintains cellular diversity while ensuring uniform target-gene disruption, avoiding clonal selection biases. Derived from the Raji Burkitt??s lymphoma line, this product is designed for advanced research on nuclear envelope biology and B-cell signaling.
The Raji parent cell line is an EBV-positive Burkitt??s lymphoma of B lymphocyte origin, characterized by high proliferation and continuous suspension growth. As a model for antibody production and antigen presentation, Raji cells are widely used in immunology and cancer research. The EBV-driven background provides a relevant context for studying oncogenic signaling and lymphocyte transformation. Knockout of EMD in these cells enables investigation of nuclear architecture in a malignant B-cell setting.
Emerin is an inner nuclear membrane protein that anchors chromatin to the nuclear lamina and modulates mechanotransduction. It interacts with lamin A/C, BAF (BANF1), nesprins, and Lmo7, forming part of the LINC complex. Emerin is regulated by mechanical stress and Src family kinases, and it participates in Wnt/??-catenin and TGF-?? pathways. It directly binds ??-catenin, influencing transcription of target genes like MYC and CCND1, and interacts with SMAD2/3 in TGF-?? signaling. Additionally, emerin affects YAP/TAZ activity, linking nuclear mechanics to transcriptional regulation. Its knockout disrupts these interconnected networks, making it a valuable tool for dissecting emerin-dependent signaling.
In Raji B cells, loss of emerin is anticipated to perturb nuclear envelope integrity and mechanosensitive pathways, potentially altering proliferation and gene expression. Disrupted Wnt/??-catenin signaling may downregulate MYC, affecting cell cycle progression, measurable via Ki-67 flow cytometry. The model also allows examination of how nuclear architecture influences B-cell functions and lymphomagenesis. It serves as a platform to study the role of emerin in B-cell malignancies and to evaluate therapeutic responses in a mechano-sensitive context.
Key applications include nuclear envelope studies, Emery-Dreifuss muscular dystrophy modeling, mechanotransduction in lymphocytes, and Wnt signaling in lymphoma. Compatible techniques encompass immunofluorescence for lamin A/C, immunoblotting for emerin, transcriptomic analysis by RNA-seq, ChIP-qPCR for ??-catenin targets, and flow cytometry for proliferation and apoptosis. Drug sensitivity assays with doxorubicin can be performed to assess chemoresistance. The polyclonal format supports population-based screens without clonal artifacts. For more information, contact Ascent Research.
