KAT7 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of AGS human gastric adenocarcinoma cells with targeted KAT7 disruption. This heterogeneous model avoids clonal artifacts and enables population-level studies of KAT7-dependent chromatin regulation, cell cycle progression, and DNA replication. Each lot is validated for target gene disruption, ensuring reliable functional analyses.
The AGS cell line is a widely used epithelial model of human gastric adenocarcinoma featuring wild-type p53. It is extensively employed to study gastric tumor biology, signal transduction, and chemotherapeutic responses, and its functional p53 status makes it ideal for dissecting p53-dependent apoptosis and cell cycle checkpoints.
KAT7 (HBO1/MYST2) is the catalytic subunit of the HBO1 acetyltransferase complex, which acetylates histone H4 at K5, K8, and K12 and H3 at K14, relaxing chromatin to promote transcription and DNA replication origin licensing. The complex assembles via scaffold proteins ING4/5, JADE1/2/3, and BRPF1. KAT7 also directly acetylates p53 at K120 and K164, enhancing transcription of pro-apoptotic targets such as CDKN1A (p21), BAX, and PUMA. Upstream, KAT7 is regulated by E2F transcription factors, CDK2/4 kinases, and DNA damage signals through ATM/ATR. It facilitates MCM2-7 loading onto origins through interactions with ORC1-6, CDC6, and CDT1, linking chromatin modification to replication.
In gastric cancer, KAT7??s acetylation of p53 at K120/K164 is critical for tumor suppression. AGS cells, with wild-type p53, are ideal for studying how KAT7 loss impairs p53-mediated apoptosis and cell cycle arrest under stress. KAT7 knockout is expected to reduce H4 acetylation, alter chromatin accessibility, impair origin firing, and attenuate p53 transcriptional output, providing a model to dissect chromatin-p53 crosstalk and identify therapeutic vulnerabilities.
These cells suit cancer epigenetics research, drug target validation, and mechanistic studies of DNA replication and apoptosis. Key applications include Western blotting for acetyl-H4 and acetyl-p53, RT-qPCR of CDKN1A, BAX, and PUMA, and functional assays such as MTT proliferation, Annexin V/PI apoptosis, PI cell cycle, EdU incorporation, colony formation, and xenograft tumor growth. For specifications and ordering, contact Ascent Research.
