The NSD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphoblastoid cell line. This product serves as a loss-of-function model for the NSD1 gene, generated through CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with targeted disruption of the NSD1 locus. The polyclonal format reflects a mixture of edited alleles, providing a population-level representation of NSD1 deficiency suitable for functional genomic studies.
The Raji cell line was established from a Burkitt lymphoma patient and is widely used as a model for B cell malignancies and Epstein-Barr virus (EBV)-associated lymphomagenesis. These cells are EBV-positive and express hallmark B cell surface markers, including CD19, CD20, and surface IgM. Raji cells retain key signaling pathways relevant to B cell receptor signaling and oncogenic transformation, making them a valuable host for investigating the molecular mechanisms underlying lymphoma development and progression.
NSD1 encodes a histone-lysine N-methyltransferase that catalyzes dimethylation of histone H3 at lysine 36 (H3K36me2), a modification linked to transcriptional elongation. As a transcriptional coregulator, NSD1 interacts with nuclear receptors such as androgen receptor (AR), retinoic acid receptor alpha (RAR??), and thyroid hormone receptor beta (TR??). It binds cofactors including Nizp1 (ZNF496), FHL2, and BRD4, and associates with RNA polymerase II. NSD1 is regulated by MAPK and PI3K-AKT pathways and controls expression of target genes like HOXA9, MYC, and CCND1.
In the context of Raji B lymphoma cells, disruption of NSD1 eliminates its methyltransferase activity, leading to a profound loss of H3K36me2 chromatin marks. This epigenetic alteration remodels the transcriptional landscape, notably reducing expression of HOXA9 and MYC, which are key drivers of proliferation and survival in hematopoietic malignancies. Consequently, NSD1 knockout Raji cells may exhibit impaired cell growth, altered cell cycle progression, and enhanced apoptotic responses, providing a physiologically relevant system to dissect NSD1-dependent oncogenic programs and epigenetic dependencies in B cell lymphomas.
These cells support applications in cancer epigenetics, functional genomics, and drug discovery. Key techniques include ChIP-seq for H3K36me2 profiling, Western blotting for NSD1, and RT-qPCR/RNA-seq for gene expression analysis. Functional assays such as MTS, flow cytometry-based apoptosis, and colony formation can measure phenotypic outcomes. They also enable exploration of nuclear receptor signaling and epigenetic vulnerabilities in lymphoma. For additional information, contact Ascent Research.
