The H4C1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This product features targeted disruption of the H4C1 gene, which encodes a core replication-dependent histone H4 variant. As a polyclonal population, the cells carry a heterogeneous spectrum of CRISPR-induced edits within H4C1, providing a versatile loss-of-function model for studying histone H4 biology without monoclonal selection artifacts. This knockout model enables investigation of H4C1-dependent processes in a gastric epithelial context.
The parental AGS cell line originates from a human gastric adenocarcinoma and displays adherent epithelial morphology. Widely utilized as a model for gastric cancer, these cells recapitulate aspects of epithelial barrier function and uncontrolled proliferation characteristic of gastric malignancies. The AGS background provides a clinically relevant platform for exploring oncogenic mechanisms and therapeutic vulnerabilities in the stomach. Combined with H4C1 knockout, this system is particularly suited for dissecting epigenetic contributions to gastric adenocarcinoma progression.
H4C1 encodes histone H4, a core nucleosome component essential for chromatin organization. Its expression is replication-dependent, controlled in S phase by E2F transcription factors and the NPAT/HiNF-P complex downstream of Cyclin E/CDK2, with SLBP coordinating mRNA processing. H4 protein forms octamers with H2A, H2B, and H3 and is deposited onto DNA by chaperones including CAF-1, ASF1, and NAP1. This orchestrated assembly is vital for nucleosome formation, genomic stability, and epigenetic regulation. Knockout of H4C1 disrupts nucleosome occupancy, leading to aberrant chromatin accessibility, transcriptional dysregulation, and replication stress.
In the AGS gastric adenocarcinoma model, H4C1 loss-of-function provides a means to interrogate how replication-coupled histone supply impacts cancer cell behavior. By impairing proper chromatin assembly, the knockout can reveal synthetic lethal interactions, epigenetic vulnerabilities, and altered DNA damage responses unique to gastric epithelial cells. This model enables researchers to connect histone dynamics with oncogenic signaling pathways and identify potential therapeutic targets in gastric cancer. Because H4C1 is a core histone, its disruption broadly affects cell cycle progression and genome integrity, making it a powerful tool for studying epigenetic dysregulation in a disease-relevant context.
Typical applications include functional genomics using RNA-seq and ChIP-seq, cell cycle flow cytometry, proliferation assays, colony formation, migration/invasion studies, and drug sensitivity profiling. These cells enable population-level analysis of H4C1 loss without clonal artifacts, facilitating reproducible studies of histone biology. For more information or custom inquiries, please contact Ascent Research.
