The MSL3 Knockout Raji Polyclonal Cells consist of a heterogeneous CRISPR/Cas9-edited Raji B-lymphocyte population with targeted disruption of the MSL3 gene. This polyclonal knockout model is designed for loss-of-function studies of MSL3-mediated chromatin regulation, avoiding clonal selection bias and enabling robust assessment of gene expression and phenotypic changes at the population level.
The Raji cell line originates from a Burkitt??s lymphoma patient, maintains an EBV-positive, immortalized B-cell phenotype, and is a staple in immunological and oncological research. Its well-characterized biology and ease of culture make it an excellent host for gene-editing approaches, providing a physiologically relevant context to investigate epigenetic contributions to B-cell malignancies, proliferation, and DNA damage responses.
MSL3 is a key scaffold component of the male-specific lethal (MSL) histone acetyltransferase complex, assembling MSL1, MSL2, and the catalytic subunit KAT8 (MOF). This complex catalyzes the specific acetylation of histone H4 at lysine 16 (H4K16ac), a mark associated with chromatin relaxation and transcriptional activation. MSL3 interacts directly with KAT8 and is essential for complex integrity; its knockout abolishes H4K16ac deposition, leading to nucleosomal compaction, altered chromatin accessibility, and global changes in gene expression. Downstream consequences include dysregulation of pathways governing cell cycle progression, apoptosis, and DNA damage repair.
In Raji B cells, MSL3 disruption provides a powerful model to study epigenetic dysregulation in hematologic cancers. Burkitt??s lymphoma frequently exhibits aberrant histone modification patterns, and the MSL complex contributes to maintaining oncogenic chromatin states. Loss of MSL3 may attenuate proliferation, induce differentiation, or enhance sensitivity to genotoxic stress, revealing chromatin-based therapeutic vulnerabilities. Moreover, the EBV-positive background permits investigation of crosstalk between viral latency programs and host chromatin modifiers.
This knockout pool supports a wide array of experimental workflows, including Western blotting and RT-qPCR to confirm MSL3 ablation and H4K16ac reduction, ChIP-qPCR to assess locus-specific acetylation, and RNA-seq for transcriptome-wide profiling. Functional assays such as flow cytometry for cell cycle distribution, proliferation measurements, and apoptosis detection are readily applicable. Additionally, the polyclonal nature of the cells makes them well-suited for drug screening and target validation studies, where population-level responses are critical. For further technical details or to discuss customized applications, please contact Ascent Research.
