DMTN Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population with targeted disruption of the human DMTN gene in Raji B lymphocytes. This pool of gene-edited cells avoids clonal selection, preserving editing-outcome diversity for functional studies. DMTN encodes dematin, an actin-bundling protein essential for membrane-cytoskeletal linkage. The knockout model enables investigation of cytoskeletal dynamics and signaling in a B-cell context.
The Raji parental line originates from an EBV-positive Burkitt lymphoma and represents a classic B-lymphocyte model. These suspension cells are capable of antibody production, antigen presentation, and immune memory functions. Their lymphomagenic background, driven by MYC deregulation, provides a relevant system to study how DMTN loss impacts B-cell transformation and cytoskeletal integrity.
Dematin, the product of DMTN, crosslinks actin filaments and anchors the spectrin?Cactin junctional complex to the membrane. Its regulation involves integrin signaling, RhoA, Rac1, Abl kinase, and Src family kinases. Downstream, it stabilizes the spectrin network and influences membrane deformability. Key binding partners include spectrin, actin, adducin, tropomyosin, tropomodulin, and protein 4.1. Loss of dematin is predicted to disrupt RhoA/ROCK-mediated contractility and actin polymerization, compromising cytoskeletal organization and cell shape.
In B lymphocytes, DMTN knockout impacts immune synapse formation, antigen gathering, and migration by altering actin dynamics and membrane mechanics. This model facilitates dissection of cytoskeletal contributions to Burkitt lymphoma pathogenesis and can mirror hereditary elliptocytosis defects. The polyclonal design also permits analysis of response heterogeneity across the population.
Researchers can employ these cells in Western blotting for dematin, immunofluorescence for F-actin, and actin polymerization assays. Flow cytometry assesses morphology, transwell assays evaluate migration, and co-immunoprecipitation confirms spectrin interactions. Atomic force microscopy quantifies membrane stiffness. Applications include B-cell cytoskeleton studies, signaling pathway mapping, and drug target validation. For additional information, please contact Ascent Research.
