The FZD3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the FZD3 gene in the Raji B lymphocyte cell line. This product provides a genetically heterogeneous loss-of-function model, suitable for studying FZD3-dependent processes without clonal selection artifacts. The polyclonal format ensures retention of a broad genetic background, enabling robust and reproducible investigation of Frizzled-3 receptor function in a human B cell context. As a ready-to-use reagent, it facilitates direct interrogation of Wnt signaling networks in immunologically relevant cells.
Derived from a male patient with Burkitt lymphoma, the Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphocyte model characterized by the t(8;14) MYC translocation. These cells exhibit a B cell phenotype capable of antibody secretion and are widely utilized in studies of humoral immunity, lymphomagenesis, and signal transduction. The EBV latent gene expression program sustains continuous proliferation, making Raji cells an ideal host for CRISPR-mediated gene disruption. Their well-documented karyotype and established culture conditions support reproducible experiments in cancer biology and immunology.
The FZD3 gene encodes a seven-transmembrane Frizzled receptor that selectively binds Wnt ligands, including WNT5A and WNT11, to activate non-canonical planar cell polarity (PCP) signaling. FZD3 forms complexes with Dishevelled (DVL), VANGL2, and ROR2 at the membrane, orchestrating downstream events such as RAC1-mediated cytoskeletal reorganization and JNK-dependent transcriptional responses. Knockout of FZD3 disrupts this molecular network, leading to impaired activation of JNK, c-JUN, and Rho GTPases, which are critical effectors controlling cell polarity, migration, and morphological changes. Consequently, this model allows precise dissection of FZD3 contributions to Wnt/PCP signaling independent of ??-catenin-dependent pathways.
In Raji B lymphocytes, FZD3 ablation is expected to compromise PCP-directed processes essential for lymphocyte function, such as directed migration, uropod formation, and immune synapse organization. Given the role of Wnt signaling in hematopoietic malignancies, this knockout model enables investigation of how FZD3 loss influences oncogenic phenotypes including proliferation, survival, and invasive behavior in a MYC-driven lymphoma background. The interaction between FZD3 and core PCP components VANGL2 and DVL in these cells provides a unique platform to study polarity signaling in the context of B cell biology and lymphomagenesis.
Researchers can employ this polyclonal knockout population for functional analysis of FZD3 in Wnt signaling, with applications such as Western blotting of phospho-JNK and c-JUN to assess pathway activity, RT-qPCR profiling of Wnt target genes, and immunofluorescence staining of polarity markers like VANGL2. Flow cytometry can quantify surface receptor expression changes, while transwell and scratch assays evaluate migration. Additionally, this model supports studies on the intersection of FZD3 with lymphoma progression and therapeutic targeting. For further details or to inquire about this product, please contact Ascent Research.
