The FHOD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Raji B lymphocyte line. This product features targeted disruption of the FHOD1 gene, which encodes a formin family actin nucleation factor, providing a powerful tool for investigating actin cytoskeleton dynamics and RhoA signaling in a lymphocytic background. The polyclonal knockout approach ensures a heterogeneous genetic disruption that reflects the natural variability of CRISPR editing, making it suitable for studying population-level phenotypes without the bottleneck effects of clonal selection.
Raji cells are a well-characterized human B lymphocyte line originally isolated from a Burkitt lymphoma patient. These suspension cells exhibit an Epstein?CBarr virus (EBV)-positive phenotype and retain many features of mature B cells, including the ability to produce antibodies and present antigens. Their robust growth and stable karyotype make them a popular model for lymphoma biology, immunology, and cytoskeletal studies. The EBV-immortalized background additionally provides a context for exploring viral?Chost interactions, particularly those involving the actin cytoskeleton.
FHOD1 is a diaphanous-related formin acting downstream of RhoA. Upon activation by RhoA and ROCK, it promotes actin nucleation and polymerization, assembling linear actin filaments. FHOD1 interacts with profilin and Src family kinases, and associates with Rac1. The RhoA/ROCK?CFHOD1?Cactin axis also regulates SRF-mediated transcription via the MAL cofactor, coupling cytoskeletal dynamics to gene expression. Thus, FHOD1 disruption impairs cell migration, adhesion, and cytokinesis.
In the context of Raji B lymphocytes, FHOD1 knockout has profound implications. B cells rely on dynamic actin remodeling for immune synapse formation, antigen internalization, and migration within lymphoid tissues. The EBV-positive Raji model allows investigation of how viral factors may co-opt formin-mediated actin assembly to enhance cell proliferation or immune evasion. Loss of FHOD1 is expected to attenuate RhoA-driven cytoskeletal responses, potentially affecting lymphoma cell invasiveness, cell cycle progression, and the ability to form productive interactions with T cells. This model thus serves as a valuable platform for dissecting the molecular underpinnings of B-cell malignancies and immune dysfunction.
Researchers can utilize FHOD1 Knockout Raji Polyclonal Cells in a wide array of experimental settings. Typical applications include evaluating the role of formin-dependent actin polymerization in B-cell migration via transwell assays, visualizing F-actin organization using phalloidin staining and fluorescence microscopy, and assessing cell cycle distribution by flow cytometry. The polyclonal population is also suitable for biochemical studies such as western blotting to confirm FHOD1 ablation and co-immunoprecipitation to explore impaired RhoA?CFHOD1 interactions. Moreover, these cells are an ideal system for screening compounds targeting the actin cytoskeleton in lymphoma. For technical support or ordering information, please contact Ascent Research.
