The DNMBP Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, in which the DNMBP gene has been disrupted to create a loss-of-function model. This polyclonal format provides a heterogeneous pool of edited cells, enabling robust pooled functional assays without single-cell cloning. The knockout disrupts the scaffolding protein DNMBP, a critical Cdc42 effector that coordinates actin cytoskeleton remodeling and membrane trafficking.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma line widely used to study B lymphocyte biology, including antibody production, antigen presentation, and adaptive immune responses. Their transformed yet functionally relevant phenotype makes them a versatile platform for investigating signaling pathways, endocytosis, and cytoskeletal dynamics in a malignant B cell context.
DNMBP functions as a scaffold that directly links activated Cdc42-GTP to actin polymerization by recruiting N-WASP and the Arp2/3 complex. It interacts with dynamin-1/2, WIP, clathrin, AP-2, and Ena/VASP, acting downstream of B cell receptor activation, growth factor receptors, and integrin signaling. Through these interactions, DNMBP drives membrane invagination during receptor-mediated endocytosis and reinforces tight junctions by organizing ZO-1 and occludin at cell?Ccell contacts, thereby regulating dynamic cytoskeletal responses and barrier integrity.
In the Raji B cell model, DNMBP knockout perturbs actin-dependent processes essential for immune function, such as B cell receptor internalization, antigen uptake, and immune synapse formation. Loss of this scaffold compromises the coupling of Cdc42 signaling to actin polymerization, altering endocytic trafficking and potentially impairing cell adhesion and polarity. These defects provide a physiologically relevant system to dissect how DNMBP integrates cytoskeletal and membrane remodeling in lymphocytes.
This knockout product is well-suited for a range of applications, including analyzing actin dynamics in B lymphocytes, screening cytoskeletal modulators, and studying endocytosis in lymphoma biology. Representative assays include western blotting for DNMBP, immunofluorescence of the actin cytoskeleton, flow-cytometric measurement of surface receptor internalization, co-immunoprecipitation of Cdc42/N-WASP complexes, RT-qPCR for target genes, apoptosis assays, and drug sensitivity screens. It also serves as a cellular model for investigating DNMBP-related pathologies such as nephrotic syndrome and autoimmune disorders. For further information and technical inquiries, please contact Ascent Research.
