This product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the euchromatic histone-lysine N-methyltransferase 1 (EHMT1) gene in Raji cells. These polyclonal knockout Raji cells serve as a loss-of-function model to study the role of EHMT1 in B-lymphocyte biology. Using CRISPR/Cas9-mediated gene disruption, the heterogeneous pool of edited alleles permits averaged functional analyses without clonal isolation, ideal for initial epigenetic screens.
Raji cells are an Epstein-Barr virus (EBV)-positive suspension B-lymphoblastoid line derived from Burkitt??s lymphoma. This immortalized model retains key B-cell features, including active immunoglobulin expression and apoptosis susceptibility, making it widely used for B-cell malignancy, EBV latency, and signaling research. The EHMT1 knockout in Raji offers a relevant background to study epigenetic modifiers in lymphomagenesis.
EHMT1 encodes a histone methyltransferase catalyzing mono- and dimethylation of H3K9 (H3K9me1/2) to establish repressive chromatin. Typically complexed with EHMT2/G9a and recruited by ATF7IP, it is regulated by AKT, CDK1/cyclin B, and MYC, and represses CDKN1A, CDH1, and BCL2L11. EHMT1 interacts with DNMT1, DNMT3A, and HP1 to coordinate DNA methylation and gene silencing, and it modulates Wnt/Notch signaling through TCF/LEF repression.
In Raji B-lymphoma cells, EHMT1 knockout ablates H3K9me1/2 deposition, potentially reactivating silenced tumor suppressors and altering cell fate. This model is valuable for probing epigenetic dependencies in lymphomagenesis, with expected increases in p21 and E-cadherin affecting proliferation and apoptosis. Validation can employ ChIP-qPCR for H3K9me2, Western blotting, and flow cytometry. The polyclonal format mirrors tumor heterogeneity, enabling averaged functional readouts.
Typical applications include investigating epigenetic regulation in B-cell lymphoma, validating EHMT1 inhibitors, and studying H3K9 methylation-dependent gene silencing. The EHMT1 knockout Raji polyclonal cells are ideal for RNA-seq, ChIP-qPCR, proliferation and apoptosis assays, and drug sensitivity profiling. They facilitate synthetic lethal interaction studies and evaluation of epigenetic combination therapies. For technical inquiries or custom projects, please reach out to Ascent Research.
