The DTNA Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphoblastoid cell line, offering a powerful tool for investigating the loss of function of the DTNA gene. This product comprises a heterogeneous pool of cells bearing CRISPR/Cas9-mediated disruptions in the DTNA locus, enabling studies of alpha-dystrobrevin ablation without the constraints of clonal selection. The polyclonal format provides a representative range of editing outcomes, facilitating phenotypic assays that reflect population-level gene knockout effects.
The Raji host cell line is an Epstein-Barr virus (EBV)-transformed B lymphocyte line originally derived from a patient with Burkitt’s lymphoma. These suspension lymphoblastoid cells express characteristic B-cell markers including CD19 and CD20, and harbor the EBV genome. Raji cells are widely employed as a model for B-cell lymphoma and in immunological assays, making them a well-characterized platform for dissecting signaling pathways and cytoskeletal organization in B lymphocytes.
DTNA encodes alpha-dystrobrevin, a cytoplasmic scaffolding protein that is a core component of the dystrophin-associated glycoprotein complex (DGC). Alpha-dystrobrevin directly interacts with dystrophin (DMD) and utrophin (UTRN) to anchor the actin cytoskeleton to the extracellular matrix, and binds syntrophins (SNTA1, SNTB1), dystrobrevin binding protein 1 (DTNBP1), and sarcospan (SSPN). Through these interactions, DTNA plays a critical role in mediating signal transduction events downstream of integrin and focal adhesion pathways, and facilitates the clustering of ion channels at membrane specializations. Disruption of DTNA is expected to dismantle DGC integrity, leading to altered actin dynamics and impaired linkage between the cytoskeleton and the cell surface.
In the context of Raji B cells, knockout of DTNA disrupts the DGC-mediated scaffolding that normally coordinates cell adhesion, migration, and signal transduction. Given that B lymphocytes rely on dynamic cytoskeletal reorganization for immune synapse formation and trafficking, the DTNA knockout model provides a unique tool to dissect dystrophin complex functions in non-muscle cells. This model is particularly relevant for exploring molecular mechanisms underlying left ventricular noncompaction cardiomyopathy, X-linked dilated cardiomyopathy, and muscular dystrophies, as it allows investigation of conserved DGC pathways in a hematopoietic background.
Researchers can utilize these polyclonal knockout cells in a broad array of assays, including Western blot analysis of DGC components, immunofluorescence microscopy to visualize actin cytoskeleton architecture, cell adhesion and migration assays, flow cytometric profiling of surface markers, RNA-seq transcriptome analysis, and co-immunoprecipitation to study residual complex formation. The product is well-suited for drug screening campaigns targeting cardiomyopathy-related pathways and for functional studies of B-cell adhesion and migration. For further technical specifications or custom inquiries, please contact Ascent Research.
