The NSD3 Knockout Raji Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphocyte line, in which the NSD3 gene has been disrupted to create a loss-of-function model. The knockout pool is generated by transient delivery of Cas9 nuclease and guide RNAs targeting NSD3, followed by selection to enrich for edited cells. This polyclonal format maintains population heterogeneity and avoids the selection biases inherent to clonal isolation, providing a robust tool for NSD3 functional studies without a fixed clonal genotype. Cells are supplied as a cryopreserved mixed population ready for suspension culture recovery.
The Raji cell line is a well-established B lymphocyte model established from a Burkitt lymphoma patient. Raji cells are Epstein?CBarr virus (EBV)-positive and grow as lymphoblastoid suspensions. They are extensively used in immunological studies, EBV latency research, and investigations of B?cell receptor signaling. The EBV?positive background adds a layer of complexity that allows examination of viral?Chost interactions in the context of epigenetic processes. As a suspension culture, Raji cells are amenable to high?throughput assays common in functional genomics.
NSD3 encodes a histone lysine methyltransferase that catalyzes dimethylation of histone H3 at lysine 36 (H3K36me2), a mark of transcriptionally active chromatin. It is activated downstream of nuclear receptors RAR?? and ER?? and functions within the FGFR1 and MYC transcriptional networks. The methyltransferase interacts with BET bromodomain protein BRD4, histone deacetylases HDAC1/2, and, in translocation-driven cancers, the NUT fusion partner. Through these interactions, NSD3 promotes H3K36me2 deposition at promoters of oncogenes such as MYC and CCND1, recruiting co?activator complexes that facilitate RNA Polymerase II elongation. Thus, NSD3 acts as a chromatin?level regulator that tunes proliferation and survival gene programs.
In Raji B?lymphoma cells, NSD3?mediated H3K36me2 contributes to oncogenic MYC transcriptional networks. Disrupting NSD3 enables dissection of its role in lymphoma cell proliferation, survival, and signaling responses. The EBV?positive status of Raji further permits study of potential NSD3 involvement in viral latency and EBV?regulated gene expression. This polyclonal knockout model therefore provides a platform to investigate NSD3 function in a transformation?relevant B?cell environment that retains both Burkitt lymphoma pathology and viral epigenetic interactions.
Key applications include RNA?seq and ChIP?seq for transcriptomic and epigenomic profiling, western blotting for NSD3 and histone modifications, proliferation (MTS/ATP), colony formation, and flow cytometry?based cell cycle/apoptosis assays. Drug sensitivity, migration, and invasion assays can further characterize NSD3?dependent phenotypes. This product is also suitable for CRISPR screens and preclinical evaluation of NSD3?targeted inhibitors in a lymphoma model. For technical inquiries, please contact Ascent Research.
