FUBP3 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-mediated FUBP3-disrupted polyclonal population derived from the Raji B lymphocyte line. As a polyclonal knockout, this product maintains genetic heterogeneity while eliminating target gene function, making it suitable for bulk biochemical and screening assays that do not require monoclonal expansion. Loss of FUBP3 expression is achieved through genome editing, providing a reliable model for investigating FUBP-dependent transcriptional pathways.
Raji cells originate from a Burkitt’s lymphoma patient and are Epstein-Barr virus (EBV)-immortalized, retaining B-cell characteristics such as antibody production and antigen presentation. This widely used lymphoblastoid line supports robust growth in culture and serves as a standard model for B-cell malignancies and humoral immunity studies. The EBV-positive status mimics lymphomagenic conditions, providing a relevant context for studying oncogene function.
FUBP3 binds the FUSE upstream element in the MYC promoter, acting as a transcriptional activator to drive c-MYC expression. Upstream signals including BCR signaling and IL-4 stimulation modulate this activity. FUBP3 cooperates with general transcription factor TFIIH, RNA helicases, and FUBP1 to assemble transcription complexes. The resulting MYC protein orchestrates cell cycle progression by upregulating CCND2 and CDK4, activating E2F-dependent transcription. This FUBP3?CFUSE?CMYC axis integrates mitogenic cues to control proliferation.
In Raji cells, FUBP3 knockout reduces c-MYC transcription, diminishing the expression of MYC targets and impairing cell cycle progression. Heightened apoptosis susceptibility reflects the MYC addiction typical of Burkitt’s lymphoma, making this model valuable for examining oncogene dependency and therapeutic disruption of the MYC network in B-cell lymphomas. Additionally, the polyclonal nature preserves cellular heterogeneity, facilitating population-level readouts.
This polyclonal knockout is suited for studies of FUSE-binding protein biology, dissection of MYC transcriptional regulation, and compound screening for MYC modulators. Assays include western blotting for MYC and downstream effectors, RT-qPCR for MYC mRNA, flow cytometric cell cycle analysis (PI staining), proliferation (MTT), and apoptosis (Annexin V/7-AAD). RNA-seq and ChIP-qPCR at the MYC FUSE enable transcriptomic and binding-site analyses. For further assistance, contact Ascent Research.
