KAT6A Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the KAT6A gene in Jurkat T lymphocytes. This loss-of-function model enables study of KAT6A in hematopoietic processes and leukemogenesis. The polyclonal format reflects heterogeneous editing, avoiding clonal bias. The polyclonal cell population preserves the diversity of editing outcomes, offering a representative model for pooled functional screens and biochemical assays and drug target validation.
Jurkat cells are immortalized T lymphocytes derived from an adolescent male with acute T cell leukemia. Widely used for studying T cell signaling, apoptosis, and T-ALL pathobiology, these cells feature activated NOTCH1 and rapid suspension growth. Their relevant oncogenic context makes them ideal for examining epigenetic drivers of leukemia. Jurkat cells exhibit key features of T cell receptor cascades and serve as a standard model for T cell leukemia, providing a pertinent background for investigating KAT6A-mediated transcriptional regulation in a malignant setting.
KAT6A is a histone acetyltransferase that acetylates histones H3 and H4, functioning as a transcriptional coactivator within a complex containing BRPF1, ING5, and MEAF6. It is regulated by upstream factors RUNX1, PU.1, NOTCH1, LEF1, and MLL1, and it targets HOXA cluster genes, MEIS1, CDKN2A, CDKN1A, and MYC. KAT6A links developmental signals to chromatin remodeling, driving gene expression critical for hematopoiesis and stem cell maintenance.
In Jurkat cells, KAT6A knockout enables dissection of its role in T cell leukemia. Loss of function reduces histone acetylation at target loci, impairs HOXA/MEIS1 expression, and may alter p53 pathway activity. This model reveals how KAT6A sustains oncogenic programs driven by NOTCH1 and RUNX1. By disrupting KAT6A, researchers can explore its impact on proliferation, differentiation, and survival in a leukemic T cell context, as well as its role in epigenetic dysregulation. The polyclonal population is suited for studying phenotype variability and pooled screens.
This knockout model supports functional genomics, leukemia research, and epigenetic drug discovery. Experimental approaches include ChIP-qPCR for histone acetylation at target promoters, RT-qPCR for HOXA9 and MEIS1, Western blotting for acetylation marks, flow cytometry for differentiation markers, colony-forming assays, and drug sensitivity testing with KAT6A inhibitors. These applications enable mechanistic dissection of KAT6A in T-ALL and validation of therapeutic strategies. For additional technical specifications, please contact Ascent Research.
