The FOXP1 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the FOXP1 gene has been disrupted across a heterogeneous pool of Raji B lymphocytes. This product provides a pooled loss-of-function model that preserves the diversity of editing outcomes, enabling physiologically relevant interrogation of FOXP1-dependent mechanisms without clonal selection bias. The polyclonal format ensures retention of population-level signaling heterogeneity characteristic of Burkitt lymphoma models and is suitable for functional genomics, drug screening, and pathway dissection studies.
Raji cells are an EBV-positive B-lymphoblastoid cell line established from a patient with Burkitt lymphoma. These cells exhibit mature B-cell surface markers, surface IgM expression, and constitutive activation of B-cell receptor (BCR) signaling networks. The Raji model is a well-characterized system for investigating BCR-driven proliferation, NF-??B pathway activation, and lymphomagenesis, and it is widely employed in preclinical studies of B-cell malignancies, including diffuse large B-cell lymphoma and Burkitt lymphoma.
FOXP1 encodes a forkhead box transcription factor that orchestrates transcriptional programs essential for B-cell development, differentiation, and survival. In B lymphocytes, FOXP1 is transcriptionally regulated by upstream signals from BCR-mediated kinases (SYK, BTK), NF-??B (p65/p50), and PAX5, and it is post-transcriptionally modulated by miR-34a. FOXP1 interacts with PAX5, NF-??B subunits, and HDACs to control a gene network that includes BCL6, PRDM1 (BLIMP-1), MYC, CDKN1A, and immunoglobulin genes. The mechanistic summary highlights that FOXP1 governs transcriptional outputs linking BCR, NF-??B, and PI3K/AKT/mTOR pathways to oncogenic and differentiation programs, and its disruption abrogates downstream signaling events that promote lymphomagenesis.
In the Raji background, where constitutive BCR signaling and NF-??B activity drive proliferation, FOXP1 knockout disrupts these interconnected pathways, attenuating expression of target genes such as BCL6 and MYC that are critical for lymphoma cell survival. This model captures the interplay between FOXP1 and key nodal factors like PAX5, BLIMP-1, and CDKN1A, providing a platform to dissect transcriptional hierarchies underlying B-cell malignancies. The polyclonal population avoids clonal artifacts and reflects the genetic heterogeneity inherent in tumor biology, making it a robust tool for studying drug responses and resistance mechanisms.
Typical research applications include functional genomics of B-cell lymphomas, high-throughput drug sensitivity screening, validation of therapeutic targets within the BCR and NF-??B pathways, and transcriptional regulatory network analysis. The cells are validated for use in Western blotting, RT-qPCR, RNA-seq, flow cytometry, proliferation and apoptosis assays, and phospho-signaling profiling. By combining a disease-relevant host cell line with a polyclonal knockout strategy, this product enables rigorous investigation of FOXP1 biology in lymphomagenesis and the identification of context-dependent vulnerabilities. For further information, please contact Ascent Research.
