The MARVELD2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the human MARVELD2 gene in Raji B lymphoblasts. CRISPR-mediated gene disruption generates a heterogeneous pool suitable for loss-of-function studies without clonal selection. This model is particularly relevant for investigating tight junction-associated proteins in non-epithelial cell types, including lymphocytes.
The Raji cell line, derived from Burkitt’s lymphoma, is a suspension-growing B lymphoblast model widely used in immunology and oncology for B cell biology and lymphoma studies. Its rapid proliferation and transformed phenotype facilitate genetic manipulation and functional assays. Introducing a MARVELD2 knockout in this background enables investigation of tricellulin’s impact on B cell adhesion, signaling, and malignant properties, extending tight junction research beyond epithelial systems.
MARVELD2 encodes tricellulin, an integral membrane protein at tricellular tight junctions that binds ZO-1 and occludin to maintain barrier integrity and cytoskeletal linkage. It mediates signaling downstream of TGF-??, TNF-??, IL-1??, ??-catenin/TCF, and EGFR, regulating MAPK/ERK and PI3K/Akt pathways to control proliferation and migration. In knockout Raji cells, MARVELD2 disruption is predicted to alter tight junction components ZO-1, occludin, and claudins, and to perturb ERK and Akt phosphorylation, enabling pathway dissection in a hematopoietic malignancy model.
Within the Raji cell model, the functional significance of tricellulin is largely unexplored. Although tight junction proteins are traditionally studied in polarized epithelia, emerging evidence suggests expression in hematopoietic cells and potential roles in cell?Ccell interactions and tumor progression. These knockout cells offer a system to examine how tricellulin loss affects B cell growth, migration, and chemotherapeutic response. Given MARVELD2’s association with colorectal and hepatocellular cancers, this model may reveal tumor-suppressive or oncogenic functions in lymphoma, potentially implicating tricellulin in B cell malignancy and drug resistance.
Researchers can employ these polyclonal knockout cells in multiple experimental workflows. Western blotting and RT-qPCR confirm tricellulin depletion and target expression changes; immunofluorescence microscopy assesses tight junction protein localization. Functional assays include migration/invasion chambers, barrier integrity measurements, and proliferation analysis by flow cytometry. These cells are also suitable for drug screening to restore barrier function or inhibit proliferative signaling. For more information or custom applications, please contact Ascent Research.
