The L3MBTL2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat T lymphocyte cell line. This product provides a diverse mixture of cells carrying heterogeneous L3MBTL2 gene disruptions, enabling comprehensive loss-of-function studies in a physiologically relevant T-cell environment. The polyclonal format mitigates clonal artifacts and supports robust phenotypic analyses, making it suitable for high-throughput screening and mechanistic investigations.
Jurkat cells are an immortalized human T lymphoblastoid line originally derived from a 14-year-old male with acute T cell leukemia. They constitutively express T lymphocyte surface markers CD3 and CD4 and are widely employed as a model system for T cell receptor signaling, activation, and apoptosis. Their transformed phenotype and genetic background provide a disease-relevant context for exploring epigenetic drivers of T-cell leukemogenesis and for translational research in hematological oncology.
L3MBTL2 is a chromatin-binding polycomb group protein that functions as a potent transcriptional repressor. Through its MBT repeat domains, it specifically recognizes and binds trimethylated histone H3 at lysine 27 (H3K27me3) and monomethylated/dimethylated histone H4 at lysine 20 (H4K20me1/2). This interaction facilitates chromatin compaction and stable gene silencing within polycomb repressive complex 1 (PRC1)-related pathways. L3MBTL2 directly interacts with canonical PRC1 subunits RING1B and BMI1, and its recruitment to chromatin is influenced by the histone methyltransferase EZH2. Upstream, transcription factors such as the E2F family regulate L3MBTL2 expression, while downstream targets include developmentally critical HOX gene clusters and other loci governing cell cycle progression and differentiation.
In the Jurkat background, CRISPR/Cas9-mediated knockout of L3MBTL2 ablates its repressive activity, resulting in derepression of polycomb target genes. This allows researchers to dissect the contribution of L3MBTL2 to T cell gene expression programs and to assess how its loss might promote leukemogenic transcriptional states. The model is especially pertinent for investigating epigenetic dysregulation in acute T cell leukemia, as well as broader implications for cancers harboring 22q13.31 deletions.
This knockout system is ideal for advanced research into polycomb-mediated silencing in T cell leukemia, functional characterization of L3MBTL2 in chromatin biology, and the role of MBT domain proteins in T cell development and malignant transformation. Typical experimental workflows include Western blotting for L3MBTL2 and histone modifications, RT-qPCR for target gene expression, chromatin immunoprecipitation with qPCR to assess H3K27me3 and H4K20me1/2 occupancy, and RNA sequencing for transcriptome profiling. Flow cytometry can monitor T cell activation markers, and cell proliferation or apoptosis assays provide functional readouts. For additional information or to request a quote, please contact Ascent Research.
