The DBNL Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, in which the DBNL gene has been disrupted to abrogate expression of the actin-binding adaptor protein DBNL. This polyclonal knockout model provides a pool of gene-edited cells with targeted disruption of DBNL, enabling loss-of-function studies without clonal selection artifacts. The product is designed for biomedical research on B cell receptor (BCR) signaling, cytoskeletal dynamics, and immune synapse formation.
The Raji cell line, established from a Burkitt’s lymphoma patient, is an EBV-positive suspension lymphoblastoid model widely used for mature B lymphocyte studies, exhibiting surface immunoglobulin expression, antigen presentation, and robust proliferation. Raji cells are valued for investigating B cell activation, antibody production, and BCR-mediated signaling, making them an ideal host for examining DBNL function in lymphocyte biology.
DBNL (Drebrin-like) functions as an adaptor protein coupling activated BCR signaling to actin cytoskeletal reorganization. Upon BCR stimulation, upstream Src family kinases Lyn and Syk phosphorylate effectors, leading to recruitment of DBNL to the immune synapse. There, DBNL interacts with cortactin, WASP, the Arp2/3 complex, dynamin, and actin, promoting actin polymerization and branching to facilitate immune synapse formation, receptor clustering, and endocytosis. In the canonical pathway, DBNL acts downstream of Lyn/Syk to orchestrate WASP/Arp2/3-mediated actin restructuring essential for B cell activation and antigen internalization. Thus, DBNL knockout disrupts this link, impairing BCR-induced cytoskeletal rearrangements and downstream responses.
In Raji B cells, DBNL knockout provides a physiologically relevant model for dissecting BCR signaling and actin dynamics in a lymphoma background. Disruption of DBNL compromises immune synapse integrity, antigen capture, and endocytic trafficking of BCR complexes, attenuating B cell activation and antigen presentation. This model is pertinent to lymphomagenesis research, where aberrant BCR signaling drives malignant transformation, and to immunodeficiencies and autoimmune disorders involving B cell dysregulation. Additionally, the EBV-positive status of Raji cells offers a context for studying viral oncogenesis and B cell signaling in latently infected cells.
These DBNL knockout cells can be utilized to dissect BCR proximal signaling kinetics, actin-dependent endocytic mechanisms, and immune synapse architecture via confocal microscopy. Suitable assays include western blotting for DBNL and phospho-proteins (e.g., Syk, Lyn), flow cytometry for B cell activation markers (CD69, CD86), immunofluorescence staining of F-actin and synapse proteins, co-immunoprecipitation, and endocytosis or drug sensitivity assays. Migration and invasion studies related to lymphoma are also feasible. For further information, please contact Ascent Research.
