MTF2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line. This product features targeted disruption of the MTF2 gene, which encodes a crucial non-catalytic subunit of the polycomb repressive complex 2 (PRC2). The polyclonal format provides a heterogeneous population of edited cells, enabling the study of MTF2 loss of function in a bulk culture context without clonal selection.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive lymphoblastoid cell model originally established from a Burkitt??s lymphoma patient. As a B lymphocyte cell type, Raji cells retain characteristics relevant to antibody production and adaptive immunity, making them a valuable system for investigating B cell biology and lymphomagenesis. Their rapid proliferation and well-characterized epigenetic landscape facilitate efficient functional genomics studies.
MTF2 functions as an accessory subunit of PRC2, where it potentiates EZH2-mediated trimethylation of histone H3 at lysine 27 (H3K27me3), a repressive epigenetic mark. MTF2 interacts directly with core PRC2 components EZH2, SUZ12, EED, and RBBP4, as well as accessory factors JARID2 and AEBP2. Its activity is regulated by PRC2 complex assembly and phosphorylation by AKT, and it operates downstream of MYC transcriptional control. MTF2-dependent PRC2 targeting leads to silencing of tumor suppressors such as CDKN2A and HOX gene clusters, thereby maintaining cellular proliferation and inhibiting differentiation.
In the Raji lymphoma context, loss of MTF2 disrupts efficient PRC2 recruitment to chromatin, resulting in decreased H3K27me3 levels and derepression of genes normally silenced by this machinery. This perturbation enables interrogation of PRC2-mediated epigenetic maintenance in B cell malignancies, where EZH2 gain-of-function mutations and PRC2 dysregulation are recurrent. The polyclonal knockout population thus serves as a physiologically relevant model for dissecting the contribution of MTF2 to lymphomagenesis and adaptive immune cell epigenetics.
Researchers can apply these cells to a range of experimental workflows, including chromatin immunoprecipitation followed by qPCR (ChIP-qPCR) for H3K27me3 profiling, co-immunoprecipitation to assess PRC2 complex integrity, western blotting for histone modifications, and RT-qPCR for target gene expression analysis. The model is particularly suited for validating PRC2 inhibitors and probing resistance mechanisms in lymphoma cells. By eliminating MTF2, scientists can parse its specific role within PRC2-dependent transcriptional silencing and explore its impact on proliferation and viability using EZH2 inhibitor treatments. For additional technical information or purchasing inquiries, please contact Ascent Research.
