The HAT1 Knockout Jurkat Polyclonal Cells offer a ready-to-use polyclonal knockout pool created by CRISPR/Cas9-mediated disruption of the HAT1 gene in Jurkat T-lymphoblastoid cells. This polyclonal format provides a heterogeneous loss-of-function model for probing histone acetyltransferase 1 (HAT1) functions without clonal selection bias, enabling robust phenotype assessment across a population of edited cells.
Jurkat cells are a leukemic T-cell line originating from a male acute T-cell leukemia patient. Widely employed for T-cell signaling and leukemia research, they retain functional attributes such as cytokine secretion and cytotoxic activity, making them a pertinent host for studying epigenetic regulation in immune cell biology. The Jurkat background thus allows investigation of HAT1-dependent mechanisms within a physiologically relevant T-lymphocyte context.
HAT1 is a type B histone acetyltransferase that specifically targets newly synthesized histone H4, catalyzing acetylation at lysine 5 and 12. This modification facilitates nucleosome assembly during DNA replication and repair. HAT1 operates within a multiprotein complex containing RBBP4/RbAp48 and the histone chaperones ASF1A and ASF1B, ensuring efficient H4 acetylation and deposition. Upstream, HAT1 expression is driven by E2F transcription factors and cell cycle regulatory proteins, integrating chromatin assembly with proliferation signals. The acetylated H4 is recognized by CAF-1 and HIRA complexes, which cooperate with PCNA to promote chromatin maturation and epigenetic inheritance, thus linking HAT1 to essential processes in histone modification, chromatin organization, and cell cycle progression.
In Jurkat T cells, which rapidly proliferate and depend on tight epigenetic control, HAT1-mediated H4 acetylation is critical for maintaining chromatin architecture. Loss of HAT1 in this leukemic background enables systematic exploration of how disrupted histone acetylation contributes to genomic instability and oncogenic gene expression. This polyclonal knockout model is particularly suited for studying epigenetic vulnerabilities in T-cell leukemia and for evaluating therapeutic strategies targeting chromatin-modifying enzymes.
Typical applications include western blotting to confirm HAT1 depletion and reduced H4K5/K12 acetylation, RT-qPCR for analyzing transcriptomic changes, immunofluorescence to visualize chromatin structure alterations, flow cytometry for cell cycle profiling, and in vitro histone acetylation assays to directly measure enzymatic activity. Proliferation and viability assays further enable functional interrogation of HAT1-dependent pathways. These polyclonal cells are ideal for research on epigenetic regulation, chromatin dynamics, DNA replication mechanisms, histone modification, and cancer. For additional information, please contact Ascent Research.
