The FMNL2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human Burkitt lymphoma Raji B cell line, with disrupted FMNL2 gene expression. This heterogeneous knockout pool enables loss-of-function analysis without clonal selection bias, reflecting the edited population’s overall response. By eliminating FMNL2, a formin-family actin nucleator, these cells provide a critical tool for probing cytoskeletal regulation and signaling in B lymphocytes.
The Raji cell line is an EBV-positive, surface IgM-expressing B lymphocyte line derived from a Burkitt lymphoma patient. It is widely used as an in vitro model for B cell receptor signaling, Epstein-Barr virus biology, and oncogenic transformation. Raji cells proliferate in suspension and retain key features of mature B cells, including the ability to form immune synapses and undergo cytoskeletal remodeling upon stimulation. Their genetic background offers a relevant platform for studying lymphoma biology and the molecular mechanisms underlying B cell migration and invasion.
FMNL2 encodes a formin that nucleates unbranched actin filaments, driving lamellipodia and filopodia formation. It functions downstream of Cdc42 and Rac1, is modulated by PIP2, and interacts with profilin, IQGAP1, and the exocyst complex to orchestrate actin polymerization at the plasma membrane. Through these interactions, FMNL2 couples extracellular signals to cytoskeletal dynamics, regulating cell migration, adhesion, and cytokinesis. Knockout therefore disrupts Rho GTPase-controlled actin assembly.
In the Raji B cell context, FMNL2 dysfunction is predicted to impair lamellipodial and filopodial protrusion dynamics, compromising directed migration and potentially altering B cell receptor clustering and signal transduction. Given the role of actin remodeling in immune synapse formation, these polyclonal knockout cells enable dissection of how formin-dependent actin assembly contributes to lymphocyte activation and effector functions. Moreover, because FMNL2 is implicated in metastatic progression of solid tumors, this model permits comparative studies of cytoskeletal regulation between hematopoietic and non-hematopoietic cancer cells, with specific relevance to lymphoma invasiveness.
Typical applications include Transwell migration and invasion assays, immunofluorescence for F-actin and adhesion structures, and Rho GTPase activation assays. Flow cytometry for B cell surface markers, along with Western blot and RT-qPCR for FMNL2, extend utility to studies of B cell trafficking and tumor microenvironment interactions. For further information, please contact Ascent Research.
