The DEK Knockout Raji Polyclonal Cells product comprises a heterogeneous population of Raji B lymphocytes engineered via CRISPR/Cas9-mediated gene disruption to introduce loss-of-function mutations at the DEK locus. This polyclonal knockout cell population is designed to eliminate DEK protein expression, providing a physiologically relevant model for investigating the multifaceted roles of DEK in chromatin organization, transcriptional regulation, and oncogenic signaling.
The Raji cell line was established from a Burkitt lymphoma patient and is characterized by its Epstein-Barr virus (EBV)-positive status, suspension growth, and B-lymphocyte lineage. These cells are widely used to study B-cell malignancies, immune surveillance mechanisms, and antibody production. The lymphoblastoid origin and rapid proliferation of Raji cells make them an ideal host for probing the functions of oncogenes and tumor suppressors in the context of lymphoma biology.
DEK is a non-histone chromosomal protein that functions as a transcriptional regulator and chromatin architectural factor, critically involved in DNA repair, apoptosis inhibition, and cell proliferation. DEK is transcriptionally activated by NF-??B and E2F transcription factors, and its activity is modulated by phosphorylation via CK2 kinase and PKC in response to DNA damage signals. DEK directly interacts with p53, KAP1/TIF1??, and HDAC1 to repress p53 transcriptional activity and BAX expression, while also sustaining Wnt/??-catenin target gene activation and upregulating MDM2 and survivin. In unperturbed cells, DEK contributes to the suppression of apoptosis and maintenance of genomic stability through its interactions with components of the p53, DNA damage response, and NF-??B pathways.
In Raji B lymphocytes, which originate from a Burkitt lymphoma, DEK knockout disrupts the oncogenic balance by disabling the inhibition of p53-dependent apoptosis and impairing efficient DNA repair. This loss of function leads to heightened genomic instability, accumulation of DNA double-strand breaks marked by ??H2AX, and increased sensitivity to apoptotic stimuli, as BAX expression is derepressed and downstream effectors such as survivin are downregulated. The model therefore reveals the reliance of lymphoma cells on DEK for survival and proliferation, offering insights into oncogene addiction and the molecular circuitry of B-cell malignancy.
Researchers can utilize these polyclonal DEK knockout Raji cells in diverse assays to investigate lymphoma pathogenesis, DNA damage response, and apoptosis. Western blotting and RT-qPCR confirm DEK ablation and monitor p53 pathway components (p53, BAX, MDM2), while flow cytometry quantifies apoptosis. ??H2AX immunofluorescence evaluates DNA double-strand breaks, and colony formation assays assess proliferative capacity. Drug sensitivity profiling with chemotherapeutics or targeted inhibitors can identify vulnerabilities conferred by DEK loss, informing therapeutic strategies for B-cell lymphomas. For further information or to discuss your specific research needs, please contact Ascent Research.
