The JADE1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, generated by disrupting the JADE1 gene in the HAP1 cell line. This model provides a loss-of-function system to study JADE1-dependent chromatin regulation, transcriptional control, and signaling pathways. The polyclonal nature ensures representation of diverse editing events, offering a robust tool for functional genomics without the need for single-cell cloning.
HAP1 is a near-haploid cell line derived from a male patient with chronic myeloid leukemia (CML). Its near-haploid karyotype simplifies genetic manipulation and analysis, making it an ideal host for knockout studies. The leukemic origin also provides a disease-relevant background for investigating oncogenic mechanisms and tumor suppressor-like functions of chromatin regulators.
JADE1 functions as a scaffold protein that assembles the HBO1 histone acetyltransferase complex, containing HBO1 (KAT7), BRPF1, ING5, and EAF6. This complex acetylates histone H3 at lysine 14 (H3K14ac) and histone H4, promoting open chromatin and transcriptional activation. In Wnt/??-catenin signaling, JADE1 is recruited to TCF/LEF-bound Wnt target genes, facilitating local acetylation and expression of downstream targets such as cyclin D1, c-MYC, and BCL-2. JADE1 activity is modulated by upstream regulators including CDK2 and Aurora B kinase, which can phosphorylate the scaffold to influence complex function. The scaffold function of JADE1 is essential for maintaining the integrity and acetyltransferase activity of the complex.
In the HAP1 CML background, disruption of JADE1 impairs HBO1-mediated histone acetylation and attenuates Wnt-dependent transcription, leading to altered expression of cell cycle regulators and pro-survival factors. This model enables dissection of how chromatin remodeling contributes to leukemogenesis and proliferation control. The haploid genetic environment reduces confounding alleles, allowing cleaner interpretation of genotype?Cphenotype relationships, while the cancer context provides insights into epigenetic vulnerabilities that could be exploited therapeutically.
These JADE1 knockout HAP1 cells are suitable for western blot analysis of histone acetylation marks (e.g., H3K14ac), ChIP-qPCR for H3K14ac at Wnt target genes, RNA-seq for transcriptome profiling, BrdU proliferation assays, Annexin V apoptosis assays, and Wnt luciferase reporter assays. Furthermore, they support drug response profiling to assess the role of JADE1 in epigenetic vulnerability of leukemic cells, and can serve as an isogenic control in co-culture or xenograft studies. Such applications enable research in cancer biology, chromatin remodeling, functional genomics, and epigenetic drug target validation. For further details, please reach out to Ascent Research.
