The FOXJ2 Knockout Raji Polyclonal Cells product offers a CRISPR/Cas9-mediated gene-disrupted polyclonal knockout cell population engineered from the Raji B lymphoblast cell line. This polyclonal format provides a heterogenous pool of knockout cells, enabling robust loss-of-function studies without the clonal selection biases inherent in monoclonal cell lines. The FOXJ2 gene encodes a forkhead box transcription factor implicated in tumor suppression, and its disruption creates a versatile model for dissecting transcriptional regulatory networks in B-cell lymphoma.
Raji cells are an Epstein-Barr virus (EBV)-positive suspension B lymphoblast line originally derived from a Burkitt lymphoma patient. They serve as a well-established model system for B lymphocyte biology, lymphomagenesis, and immunological research. Their rapid proliferation, stable karyotype, and EBV-driven gene expression patterns make them particularly suitable for investigating oncogenic pathways and tumor suppressor functions in a hematological context.
FOXJ2 functions as a transcriptional regulator downstream of E2F1, activating the expression of key cell cycle inhibitors and pro-apoptotic factors. It directly targets CDKN1A (p21) to enforce cell cycle arrest and BAX to promote mitochondrial apoptosis, while also modulating CCND1 (cyclin D1) expression. FOXJ2 transcriptional activity is enhanced through interaction with the coactivator CBP/p300. Knockout of FOXJ2 in this polyclonal population disrupts this network, reducing p21 and BAX expression and promoting unchecked proliferation and survival. Thus, the E2F1?CFOXJ2?CCDKN1A/BAX?CCASP3 axis is critically impaired.
In the Raji background, FOXJ2 knockout phenocopies the loss of tumor suppressor function often observed in aggressive B-cell lymphomas. The EBV-positive lymphoblastoid environment, combined with FOXJ2 depletion, amplifies proliferative signaling and survival, creating a disease-relevant platform for studying the molecular underpinnings of lymphomagenesis. This model enables dissection of how transcriptional deregulation contributes to B-cell transformation and offers a tool to evaluate therapeutic interventions aimed at restoring cell cycle control or apoptosis.
This product is ideal for a range of experimental applications, including detailed investigation of tumor suppressor mechanisms via transcriptomic profiling (RNA-seq) and targeted gene expression analysis (RT-qPCR). Protein-level validation can be performed using Western blotting for FOXJ2, p21, BAX, and caspase-3. Functional assays such as flow cytometric cell cycle and apoptosis analysis, MTT proliferation assays, and caspase activity measurements allow quantitative assessment of phenotypic consequences. For additional details or technical support, please contact Ascent Research.
