The JADE2 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line. This product provides a pool of cells harboring targeted disruption of the JADE2 gene, generated via CRISPR/Cas9-mediated gene editing. As a polyclonal population, it represents a heterogeneous mixture of knockout alleles, enabling robust loss-of-function studies without clonal selection artifacts. The knockout model is suited for investigating JADE2-dependent regulatory mechanisms in a T cell context, allowing researchers to interrogate gene function in a leukemia-relevant background. It is supplied as a ready-to-use cellular reagent for downstream molecular, biochemical, and pharmacological analyses.
The host Jurkat cell line is an extensively characterized model derived from an acute T cell leukemia patient. These cells are lymphoblasts that retain key features of T cell signaling, making them invaluable for dissecting pathways governing T cell activation, proliferation, and apoptosis. Jurkat cells have been instrumental in advancing our understanding of T cell receptor signaling, calcium flux, and transcriptional programs. Their leukemic origin also renders them highly relevant for studying oncogenic transformation and therapeutic vulnerabilities. This well-established immortalized line grows in suspension, facilitating high-throughput screening and reproducible experimental setups. As a suspension lymphoblast culture, Jurkat cells are amenable to transfection, lentiviral transduction, and flow cytometric analysis, providing a versatile platform for genetic manipulation studies.
JADE2 (Jade family PHD finger 2) functions as an essential scaffold within the HBO1 histone acetyltransferase complex, which also includes KAT7 (HBO1), ING4/5, EAF6, and MEAF6. It directs the acetylation of histone H3 and H4 tails??primarily at H3K14 and H4K8??at promoter regions of genes governing cell cycle progression and apoptosis. JADE2 is transcriptionally regulated by p53 and operates downstream of DNA damage signaling. It promotes the expression of p53 target CDKN1A (p21) and represses Wnt/??-catenin-driven genes such as AXIN2, LEF1, CCND1, and c-MYC. Through these interactions, JADE2 orchestrates chromatin remodeling that balances proliferation and cell death. Its activity is modulated by upstream stress signals and feeds into the p53 and Wnt pathways, thereby integrating epigenetic control with key signaling cascades.
In the Jurkat T cell leukemia model, JADE2 disruption abrogates HBO1-mediated histone acetylation at critical genomic loci. This loss leads to diminished expression of pro-apoptotic and cell cycle inhibitory regulators, including CDKN1A and AXIN2, while relieving suppression of CCND1 and c-MYC. Consequently, JADE2 knockout Jurkat cells exhibit enhanced survival and proliferation, mirroring the pro-leukemogenic effects observed in acute T cell leukemia. This phenotype underscores JADE2’s tumor-suppressive role within the HBO1 complex and provides a tractable system for dissecting epigenetic dependencies in malignant T cells. The polyclonal knockout population allows researchers to analyze bulk functional outcomes without the confounding influence of clonal variation, making it particularly suitable for studies requiring robust, averaged responses.
The JADE2 Knockout Jurkat Polyclonal Cells are a powerful tool for a wide range of research applications. They enable detailed investigation of leukemia cell proliferation and apoptosis by assessing changes in cell cycle distribution and apoptotic markers via flow cytometry and WST-1 assays. The model supports mechanistic studies on the HBO1 complex in T cells, including ChIP-qPCR for JADE2 binding sites and Western blotting for histone acetylation marks (H3K14ac, H4K8ac). Researchers can probe Wnt/??-catenin signaling in hematopoietic malignancies by quantifying target gene expression (AXIN2, LEF1) with RT-qPCR and performing RNA-seq for transcriptome-wide profiling. Additionally, these cells are well-suited for drug screening campaigns targeting chromatin modifiers, such as HDAC inhibitor sensitivity assays, and for exploring the epigenetic regulation of T cell activation. For further details on product specifications and customization, please contact Ascent Research.
