The FLNB Knockout Raji Polyclonal Cells comprise a heterogeneous pool of CRISPR/Cas9-edited human Raji B lymphocytes harboring targeted disruption of the filamin B (FLNB) gene. This polyclonal knockout population is designed for loss-of-function studies in suspension-adapted immune cells, providing a robust model to interrogate FLNB-dependent processes without clonal selection bias. The gene editing approach yields a mixed population with varied FLNB ablation, enabling researchers to assess functional consequences at the population level.
Raji cells are a well-established B lymphocyte line derived from an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma. These suspension cells retain key features of mature B cells, including surface immunoglobulin expression and the capacity to present antigens, making them a valuable model for studying immune response and antibody production mechanisms. Their EBV-positivity and lymphomagenic origin render them particularly useful for investigating oncogenic signaling and lymphocyte biology.
Filamin B is an actin-crosslinking protein that organizes the cortical cytoskeleton and transmits mechanical forces through integrin-based adhesion complexes. FLNB functions downstream of integrin receptors and RhoA, acting as a scaffold for FAK and RhoGEFs. It directly interacts with F-actin, FLNA, FLNC, integrins, and FBLIM1. Through these interactions, FLNB regulates the Hippo pathway effectors YAP/TAZ and TGF-??-responsive SMAD transcription factors, thereby linking mechanotransduction to transcriptional programs that control cell migration, proliferation, and adhesion. Knockout of FLNB disrupts actin network crosslinking, impairing RhoA-ROCK signaling and integrin-mediated adhesion dynamics.
In Raji B lymphocytes, FLNB is implicated in the organization of the immune synapse and signal transduction downstream of antigen receptors. Disruption of FLNB is expected to alter cytoskeletal remodeling required for efficient B cell migration, adhesion, and intercellular communication. Loss of FLNB may impair the assembly of signaling platforms at the plasma membrane, potentially affecting B cell activation, antibody secretion, and interactions with extracellular matrix components. This model therefore offers a physiologically relevant system to study how cytoskeletal integrity influences immune cell function and lymphoma progression.
Researchers can employ these FLNB knockout polyclonal cells to dissect mechanotransduction pathways in hematopoietic cells, to screen for compounds that modulate cytoskeletal dynamics, or to investigate FLNB-related pathologies such as Larsen syndrome and cancer metastasis. Typical experimental approaches include Western blot analysis for FLNB expression, immunofluorescence visualization of F-actin architecture, transwell migration assays, flow cytometric measurement of adhesion molecules, and RhoA activation assays. This polyclonal knockout model provides a versatile platform for studying the intersection of cytoskeletal organization and immune cell biology. For further technical information, please contact Ascent Research.
