FOXP2 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-mediated gene-disrupted polyclonal population generated from the Raji human B lymphocyte line, designed for loss-of-function analysis of the FOXP2 transcription factor. This product provides a heterogeneous pool of edited cells, enabling robust functional genomics screening and transcriptomic profiling without clonal selection bias. The polyclonal format supports studies where population-level responses are preferred over clonal isolates, and it is ideally suited for high-throughput applications such as CRISPR dropout screens and pooled CRISPR libraries.
The Raji parental cell line is a well-characterized Epstein-Barr virus (EBV)-positive Burkitt lymphoma model, originating from a human B lymphocyte. Raji cells exhibit robust proliferation, active immunoglobulin production, and are extensively employed in immunology and cancer biology research. Their B cell identity provides a physiologically relevant context to explore transcription factor functions that may intersect with immune signaling and lymphomagenesis, despite FOXP2??s primary association with neurodevelopmental processes.
FOXP2 encodes a forkhead box transcription factor that forms homodimers and heterodimers with FOXP1 and FOXP4, interacting with co-repressors such as CTBP1 to regulate target gene expression. Its activity is modulated by upstream signals including WNT3A/Frizzled/??-catenin/TCF/LEF, SHH/PTCH1/SMO/GLI1, and calcineurin/NFAT pathways. FOXP2 directly transcriptionally regulates a network of neurodevelopmental genes ??including CNTNAP2, SRPX2, DLX5, DLX6, UBE3A, and MET?? many of which also influence cell adhesion and synapse formation. In B lymphocytes, FOXP2 may similarly control expression of these targets, connecting WNT and calcium signaling to immune cell behavior.
Knockout of FOXP2 in Raji B cells disrupts this regulatory network, offering a model to dissect FOXP2-dependent transcriptional programs independent of neuronal context. The disruption may alter expression of CNTNAP2 and other targets, potentially affecting cell?Ccell interaction and signaling cascades that are relevant to both neural development and B cell function. This model enables investigators to study how FOXP2 loss influences pathways such as WNT/??-catenin and NFAT, which have established roles in lymphocyte activation and lymphoma progression. Consequently, it serves as a tool to explore crosstalk between transcription factor networks implicated in developmental speech-language disorders and immune cell regulation.
Researchers can employ FOXP2 Knockout Raji Polyclonal Cells in a variety of experimental workflows. Functional genomics assays, including RNA-seq and ChIP-seq, enable genome-wide analysis of FOXP2-dependent transcriptional changes and chromatin occupancy. Targeted gene expression studies by RT-qPCR and protein analysis via Western blotting facilitate validation of downstream effectors. Flow cytometry can assess surface marker alterations, while reporter gene assays quantify pathway activity. These cells are also suitable for CRISPR modifier screens and for modeling aspects of neurodevelopmental diseases in a non-neuronal system. For technical specifications and ordering information, please contact Ascent Research.
