The MLLT1 Knockout Raji Polyclonal Cells product provides a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the MLLT1 gene in the Raji cell line. This pooled knockout model is designed for researchers investigating MLLT1-dependent transcriptional regulation and its role in leukemogenesis. The polyclonal format preserves genetic heterogeneity while ensuring robust reduction of MLLT1 protein expression, making it suitable for population-based assays and functional screens.
The Raji cell line is a human B lymphocyte line derived from a patient with Burkitt lymphoma and is Epstein-Barr virus (EBV)-positive. Raji cells are widely used as a model system for B-cell malignancies and for studying EBV-associated oncogenic mechanisms. Their transformed B-cell phenotype provides a relevant cellular context for studying transcriptional abnormalities in hematological cancers, particularly those involving MLL rearrangements.
MLLT1, also known as ENL, is a transcriptional coactivator and a core component of the super elongation complex (SEC), which includes AFF4, ELL, AF9, DOT1L, and the PAF1 complex. The SEC facilitates RNA polymerase II transcriptional elongation by releasing paused polymerase. In normal physiology, MLLT1 functions downstream of ??-catenin and is regulated by DOT1L methyltransferase activity. In MLL-rearranged leukemias, oncogenic MLL-fusion proteins aberrantly recruit the SEC via MLLT1/AF9 interactions, leading to sustained activation of critical downstream targets such as HOXA9, MYC, CDK6, and CCND2, which drive cell proliferation and leukemogenesis.
In the Raji B-lymphocyte background, this MLLT1 knockout model is particularly relevant for studying the mechanistic contributions of ENL to leukemic cell maintenance and transcriptional dysregulation. The polyclonal knockout population allows for the examination of MLLT1 loss on SEC assembly and target gene expression in a cell-type-specific manner. It also provides a valuable tool for investigating the interplay between EBV-driven pathways and MLLT1-mediated transcriptional programs, as well as for screening compounds targeting the SEC or its downstream effectors.
Researchers can employ this knockout model in a wide range of experimental applications, including RNA-seq to profile transcriptomic changes, ChIP-qPCR to assess SEC occupancy at target loci, co-immunoprecipitation to study protein interactions within the SEC, and proliferation and apoptosis assays to evaluate functional consequences of MLLT1 loss. Additionally, it serves as an isogenic tool for drug screening aimed at identifying inhibitors of MLL-fusion-driven leukemogenesis. For further inquiries or detailed product specifications, please contact Ascent Research.