NSD2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji human B lymphocyte cell line, designed to disrupt the NSD2 gene (histone-lysine N-methyltransferase NSD2). This product provides a genetically defined loss-of-function model for investigating NSD2-dependent epigenetic and oncogenic mechanisms in a human B cell lymphoma background.
The Raji host cell line originates from a Burkitt lymphoma patient and is immortalized by Epstein-Barr virus (EBV). These suspension-adapted B lymphocytes serve as a well-established model for studying B cell lymphoma biology, immune responses, and viral transformation. Raji cells exhibit constitutive activation of NF-??B signaling and other pathways relevant to lymphomagenesis, making them an appropriate background for dissecting the oncogenic functions of NSD2.
NSD2 encodes a histone methyltransferase that catalyzes dimethylation of histone H3 at lysine 36 (H3K36me2), a chromatin mark recognized by bromodomain proteins such as BRD4 and critical for transcriptional activation and DNA repair. Its expression is driven by cytokine receptors and the NF-??B and PI3K/AKT pathways, with regulatory input from DNA damage sensors ATM and ATR. NSD2 forms complexes with histone deacetylases HDAC1/2, the polycomb repressive complex PRC2, and the adaptor protein 53BP1, thereby coupling epigenetic regulation to DNA double-strand break responses. Downstream, NSD2 transcriptionally regulates proliferation drivers like CCND1 and MYC, DNA repair effectors RAD51 and BRCA1, and the anti-apoptotic factor BCL2. This network integrates oncogenic signaling, chromatin remodeling, and genomic stability.
In B cell lymphomas, NSD2 is frequently overexpressed, leading to aberrant H3K36me2 deposition that drives oncogene activation and compromises DNA double-strand break repair fidelity. The Raji cell line, which harbors endogenous NSD2 expression, recapitulates aspects of this dysregulation, and its knockout allows dissection of NSD2’s contributions to proliferation, survival, and drug resistance. Thus, this polyclonal knockout model is highly relevant for elucidating the epigenetic drivers of Burkitt lymphoma and other B cell malignancies.
Researchers can employ these polyclonal knockout cells in assays such as Western blot and ChIP-qPCR for H3K36me2 quantification, RT-qPCR for target gene expression (e.g., CCND1, MYC), flow cytometry for apoptosis and proliferation, and ??-H2AX immunofluorescence for DNA damage. The model supports NSD2 inhibitor screening and drug sensitivity studies, as well as co-immunoprecipitation for interaction analysis (e.g., with HDAC1, BRD4). For further information, please contact Ascent Research.
