The MAZ Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the MAZ transcription factor gene is disrupted across the Raji B lymphocyte line. This polyclonal format comprises a heterogeneous mix of cells with different MAZ null alleles, avoiding clonal bias while enabling functional studies. The product is generated by CRISPR/Cas9-mediated gene targeting without clonal isolation, providing a versatile loss-of-function model for bulk assays.
Raji cells, derived from a human Burkitt’s lymphoma and transformed by EBV, represent a classic B-lymphoblastoid line. They display hallmark features of activated B cells, including surface immunoglobulin expression, antigen-presenting capability, and vigorous proliferation driven by MYC translocation. Their lymphoid origin and ease of culture make them widely employed in immunology and cancer research.
MAZ (MYC-associated zinc finger protein) is a transcription factor that binds GC-rich cis-regulatory elements to control gene expression. It is activated downstream of MAPK pathways, growth factor receptors, and cytokine signals. MAZ physically associates with MYC, SP1, p53, and CTCF to fine-tune transcriptional output. It directly promotes transcription of MYC and represses CDKN1A, thereby accelerating cell cycle entry, while also regulating BCL2 and HTR1A. Consequently, MAZ sits at a hub integrating proliferative and survival cues.
Disruption of MAZ in Raji cells impairs MYC transcriptional activation, leading to reduced proliferation and enhanced apoptosis susceptibility. Given the central role of MYC in Burkitt??s lymphoma pathogenesis, MAZ loss can help uncouple MYC-dependent growth from other MAZ-regulated pathways. The knockout also likely relieves CDKN1A repression and alters BCL2 levels, potentially enhancing p53-mediated responses. Thus, this model is instrumental for studying MAZ??s contribution to lymphomagenesis and cellular homeostasis.
Typical applications include chromatin immunoprecipitation (ChIP-qPCR) for MYC promoter occupancy, transcriptomic analysis via RNA-seq, protein-level validation by western blotting, and phenotypic assays such as flow cytometry for cell cycle and apoptosis markers, cell proliferation, and drug response profiling. The cells are ideal for investigating transcription factor networks and validating MAZ as a therapeutic target in lymphoma. For further details, please contact Ascent Research.
