The JADE3 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the JADE3 gene in the Jurkat T lymphocyte line. This model provides a ready-to-use tool for investigating the functional roles of JADE3 in a leukemic T cell context without researcher-performed gene editing.
Jurkat cells, derived from an acute T cell leukemia patient, serve as a standard immortalized model for studying T cell antigen receptor signaling, cytokine responses, and leukemic transformation. Their rapid proliferation and defined signaling networks suit genetic perturbation experiments probing cancer-relevant genes.
JADE3 operates as a scaffold in the HBO1 histone acetyltransferase complex, interacting with HBO1 (KAT7), BRPF1/2/3, ING4/5, and MEAF6 to acetylate histone H4 on lysines 5, 8, and 12. This complex is recruited to replication origins by ORC subunits and to promoters by transcription factors. Upstream, JADE3 is regulated by the CUL4-DDB1 E3 ligase, E2F, and MYC. H4 acetylation relaxes chromatin, enabling DNA replication licensing via MCM loading and transcription of proliferation genes such as CDT1 and CDC6, thereby promoting cell cycle progression.
In Jurkat leukemia cells, JADE3-dependent acetylation likely supports oncogenic gene expression and replication under proliferative stress. JADE3 disruption may impair HBO1 complex function, reduce H4 acetylation at specific loci, and lead to cell cycle abnormalities, decreased proliferation, or heightened DNA damage sensitivity. Thus, these cells facilitate dissection of JADE3??s role in leukemic T cell growth and chromatin dynamics.
Applications include western blotting for H4K5ac, H4K8ac, H4K12ac; RT-qPCR of replication and cell cycle genes; RNA-seq; ChIP-qPCR of H4 acetylation at promoters and origins; flow cytometry for cell cycle and apoptosis; proliferation assays; drug sensitivity testing; and co-immunoprecipitation of HBO1 complex components. These support research on chromatin regulation, leukemia biology, and epigenetic drug targeting. For more information, reach out to Ascent Research.
