The CHD1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CHD1 gene in the Raji B lymphocyte line. This ready-to-use loss-of-function model is designed specifically for investigating CHD1-dependent chromatin remodeling and transcriptional regulation within a well-established Burkitt lymphoma background, and the polyclonal format enables population-level studies without the need for single-cell cloning.
Raji cells, originally derived from an EBV-positive Burkitt lymphoma patient, are a widely used model for B-cell malignancies and Epstein-Barr virus pathogenesis. They express hallmark B-cell markers CD19 and CD20 and retain the aggressive proliferation characteristic of high-grade lymphomas. Their defined genomic and epigenomic landscape, combined with extensive literature documentation, makes Raji cells a reliable and physiologically relevant host for dissecting chromatin regulatory machinery in lymphomagenesis.
The CHD1 gene encodes an ATP-dependent chromatin remodeler that specifically recognizes histone H3 trimethylated at lysine 4 (H3K4me3) through its tandem chromodomains, thereby linking active chromatin marks to nucleosome dynamics. Mechanistically, CHD1 facilitates transcription elongation by interacting with the FACT complex (SSRP1, SPT16), the PAF1 complex, and RNA polymerase II, mobilizing nucleosomes to allow polymerase passage. It is recruited by H3K4me3 deposited by MLL-family methyltransferases and is further regulated by upstream transcription factors that modulate CHD1 expression. Downstream, CHD1 promotes expression of genes driving proliferation and, in pluripotent contexts, OCT4 and NANOG, while also contributing to DNA repair through interactions with spliceosomal components.
In the Raji Burkitt lymphoma context, CHD1 disruption is anticipated to perturb chromatin accessibility at H3K4me3-enriched promoters, leading to dysregulation of gene networks controlling B-cell activation, proliferation, and survival. This polyclonal knockout model enables systematic investigation of CHD1 dependency in EBV-positive lymphoma, evaluation of its role in maintaining the malignant phenotype, and discovery of synthetic lethal interactions with DNA-damaging chemotherapeutics or epigenetic inhibitors. Given that CHD1 is implicated in a range of cancers including prostate and leukemia, this model also serves as a broader platform for studying chromatin remodeler-driven oncogenic mechanisms. The polyclonal nature captures functional heterogeneity, an advantage for drug response screening.
Researchers can deploy these knockout cells in diverse assays: ChIP-qPCR to monitor changes in H3K4me3 occupancy, RNA-seq for transcriptome-wide profiling, and ATAC-seq to assess chromatin accessibility alterations. Functional assays such as proliferation, apoptosis, and drug sensitivity panels reveal CHD1-associated vulnerabilities, while co-immunoprecipitation confirms the loss of CHD1 interactions with factors like SSRP1 or SPT16. Flow cytometry validates sustained CD19 and CD20 expression, confirming B-cell identity. These polyclonal cells are ideally suited for pooled CRISPR screens, mechanistic validation, and drug target discovery in B-cell malignancy research. For further technical information, contact Ascent Research.
