The HAT1 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1. This product provides a heterogeneous pool of cells carrying targeted disruption of the HAT1 gene, eliminating expression of histone acetyltransferase 1. The polyclonal format preserves the genetic variability inherent to CRISPR/Cas9-mediated gene editing, enabling robust loss-of-function studies without clonal selection bias. These knockout cells serve as a powerful model for investigating the role of HAT1 in histone acetylation and chromatin dynamics.
The host cell line SK-HEP-1 is an epithelial cell line originally established from the ascitic fluid of a 52-year-old male patient with liver adenocarcinoma. This cell line is widely used in hepatocellular carcinoma (HCC) research due to its hepatic origin and malignant properties. SK-HEP-1 cells exhibit characteristic epithelial morphology and retain key oncogenic pathways, making them a valuable model for studying liver cancer biology. Their genetic background and growth characteristics are well-characterized, facilitating the interpretation of functional genomic studies.
HAT1 encodes a type B histone acetyltransferase that specifically acetylates newly synthesized histone H4 at lysine residues 5 and 12. This modification is essential for the interaction of histone H4 with the histone chaperones ASF1 and CAF-1, facilitating nucleosome assembly during DNA replication and repair. HAT1 functions downstream of cell cycle regulators such as E2F transcription factors and acts upstream of chromatin assembly pathways. The HAT1-mediated acetylation of histone H4 is critical for proper chromatin structure and genomic stability, and its dysregulation has been implicated in hepatocellular carcinoma progression.
In the context of SK-HEP-1 cells, HAT1 knockout disrupts the normal acetylation pattern of newly synthesized histone H4, impairing chromatin assembly and potentially affecting cell proliferation, cell cycle progression, and DNA repair. Since SK-HEP-1 cells are derived from liver adenocarcinoma, this model is particularly relevant for studying epigenetic alterations in HCC. The polyclonal population reflects a range of knockout efficiencies and allows examination of heterogeneous cellular responses, providing insights into the role of histone acetylation in liver cancer cell behavior and therapeutic response.
This product is ideally suited for investigations into histone modification dynamics in liver cancer, including Western blot analysis of H4K5ac and H4K12ac levels, ChIP-seq to map genome-wide changes in histone acetylation, and transcriptomic profiling via RNA-seq following HAT1 ablation. Functional studies such as cell proliferation, colony formation, and flow cytometry-based cell cycle analysis can delineate the impact of HAT1 loss on tumor cell growth. Additionally, these cells facilitate drug target validation for epigenetic therapies targeting histone acetyltransferases. Ascent Research provides this knockout model to support advanced research in cancer epigenetics and chromatin biology. For detailed product inquiries, please contact Ascent Research.
