The FOXP4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt’s lymphoma B lymphocyte line Raji. This product enables loss-of-function studies of FOXP4, a forkhead box transcription factor with repressive functions, in a lymphoma-relevant cellular background. The polyclonal nature preserves population-level heterogeneity, offering a more physiologically relevant model compared to clonal isolates, while the CRISPR/Cas9-mediated gene disruption reliably abrogates FOXP4 expression. Researchers can use these cells to investigate FOXP4-dependent regulatory mechanisms without the influence of intact gene dosage.
The Raji host cell line was established from a Burkitt’s lymphoma patient and is characterized by an EBV-positive, lymphoblastoid morphology with suspension growth. Raji cells are widely utilized as a model for B lymphocyte biology, immune surveillance, and antibody production, and their EBV status makes them particularly valuable for studying viral latency and oncogenic cooperation. The cell line retains key B cell signaling properties, providing a relevant platform to dissect transcription factor networks that govern proliferation, apoptosis, and differentiation programs in B cell malignancies.
FOXP4 functions as a transcriptional repressor of genes involved in proliferation, apoptosis, and EMT. FOXP4 is regulated by Notch (via NICD and CSL/RBP-J activating HES1), Wnt (via Frizzled/Dishevelled stabilizing Beta-catenin with TCF/LEF), and TGF-beta (via TGFBR2 and SMAD2/3/4 complexes inducing SNAI1, SNAI2, TWIST1, ZEB1). Upstream inputs also include STAT3 and NF-??B. FOXP4 interacts with Beta-catenin, TCF/LEF, CBP/p300, HDAC1, and SMAD3 to repress targets such as CDH1, VIM, SNAI1, MMP2, MMP9, p21, Cyclin D1, and Bcl-2. Knockout of FOXP4 disrupts this network, derepressing these genes and altering EMT and proliferative programs.
In the Raji lymphoma background, FOXP4 knockout provides a unique tool to dissect its role in lymphomagenesis and the interplay with EBV latency programs. As FOXP4 modulates apoptosis and EMT pathways, its loss may alter the balance between proliferative and differentiative states in B cells. The interaction with Beta-catenin and NF-??B suggests potential crosstalk with EBV-driven oncogenic pathways, making these cells suitable for investigating how viral latency factors co-opt host transcriptional repressors. Moreover, the suspension growth phenotype facilitates high-throughput applications, including drug screening and signaling analyses, directly in a lymphoma-relevant context.
These polyclonal knockout cells support a broad range of lymphoma and EMT studies. They are suitable for Western blotting, RT-qPCR, and RNA-seq to assess FOXP4 disruption and target gene changes; flow cytometry for B cell phenotypes; proliferation (CFSE, MTT), apoptosis (Annexin V), and migration/invasion assays; co-immunoprecipitation of Beta-catenin or SMAD3; and drug sensitivity screens. For further details and ordering information, please contact Ascent Research.
