The CPEB2 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes harboring a disrupted CPEB2 gene. This loss-of-function model is designed for investigating cytoplasmic polyadenylation element-binding protein 2 in B cell biology and disease. Supplied as a heterogeneous pool, the cells bypass clonal selection, facilitating rapid functional studies.
Raji cells are an Epstein-Barr virus (EBV)-positive immortalized B lymphocyte line derived from Burkitt’s lymphoma. They maintain key B cell features, including antigen presentation and antibody production, serving as a standard model for hematological malignancy research and immunology studies. The EBV-transformed background supports exploration of oncogenic signaling.
CPEB2 is an RNA-binding protein that recognizes CPE motifs in 3?? UTRs to regulate mRNA polyadenylation, translation, and stability. It directly controls p53 mRNA translation and interacts with factors such as eIF4E, PABPC1, and CPSF6. Upstream regulators include p53, AKT, and miR-107, while downstream targets include p53, CCND1, and COX-2. CPEB2 integrates signals through the PI3K/AKT/mTOR and p53 pathways, with core components like PIK3CA, AKT1, MTOR, TP53, and CDKN1A.
In Raji cells, disruption of CPEB2 impairs p53 translation, potentially altering cell cycle progression and senescence. This is significant in Burkitt lymphoma, where p53 pathway dysregulation contributes to oncogenesis. The polyclonal knockout enables dissection of how CPEB2-dependent translational control influences B cell transformation and response to targeted agents.
This polyclonal knockout model is suited for studying translational control, mRNA polyadenylation, and gene regulation in B cell malignancies. Typical applications include screening for regulators of CPEB2 activity, assessing apoptosis and cell cycle by flow cytometry, and performing genome-wide expression analyses via RNA-seq or ribosome profiling. Validation assays such as Western blot, RT-qPCR, and p53 reporter assays confirm target disruption and downstream effects. Researchers can employ these cells to explore signaling networks and drug responses in hematological cancers. For further information, please contact Ascent Research.
