The CHD7 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population designed to disrupt the CHD7 gene in the human Raji B lymphoblast cell line. This product delivers a mixed pool of edited cells carrying gene-disabling mutations, eliminating the need for single-cell cloning and enabling studies that benefit from population-level heterogeneity. The polyclonal format is particularly suited for functional genomics screens and assays requiring a broad representation of knockouts.
The Raji cell line is an immortalized B lymphocyte model derived from a Burkitt lymphoma, featuring an EBV-positive genome and the oncogenic MYC translocation t(8;14). These suspension cells are extensively used in lymphoma research, immunology, and therapeutic development due to their well-characterized signaling pathways and rapid growth. Introducing a CHD7 knockout into this context provides a tractable system for exploring the intersection of chromatin remodeling and B-cell malignancy.
CHD7 is an ATP-dependent chromatin remodeler recognizing H3K4me-modified histones and functions within BAF/PBAF complexes. It is regulated by SOX2, POU5F1, NICD, and Wnt/??-catenin, and physically interacts with BRG1 (SMARCA4) and the SET1/COMPASS complex to bridge histone methylation and nucleosome repositioning. CHD7 transcriptionally governs downstream targets including SOX9, TWIST1, BMP4, SNAI2, and POU3F2, integrating NOTCH1 signaling through MAML1 and RBPJ.
In Raji cells, loss of CHD7 likely compromises chromatin architecture at enhancers and promoters driving B-cell identity and oncogenic programs. Since MYC and NOTCH are central to Burkitt lymphoma pathogenesis, CHD7 knockout may disrupt the BAF complex??s role in sustaining aberrant gene expression, providing a model to probe epigenetic dependencies in lymphoma. This system can help identify vulnerabilities arising from altered histone modification landscapes and ATP-dependent remodeling.
Key applications include chromatin immunoprecipitation (ChIP-qPCR for H3K4me) and RNA-seq to map transcriptional changes, alongside proliferation and apoptosis assays to assess functional outcomes. The model also supports epigenetic drug screening and CHARGE syndrome research within B-cell contexts. Validation by Western blotting and RT-qPCR for targets such as SOX9 and TWIST1 is recommended. For further details, please contact Ascent Research.
