The ATF7IP Knockout HeLa Polyclonal Cells (product name ATF7IP Knockout HeLa Polyclonal Cells) represent a CRISPR/Cas9-edited polyclonal cell population designed for loss-of-function studies of the ATF7IP gene in a human cervical adenocarcinoma background. This product provides a versatile knockout model with heterogeneous editing across the cell pool, enabling robust analysis of ATF7IP-dependent functions without clonal selection bias.
These cells are derived from the HeLa cell line, an HPV-18 positive cervical adenocarcinoma epithelial line widely employed as a model for cancer biology, virology, and epigenetic research. The HeLa background offers well-characterized growth properties, genetic stability, and extensive historical reference data, making it an optimal host for investigating chromatin-based regulatory mechanisms.
ATF7IP encodes a transcriptional coregulator that physically bridges DNA methylation and histone modification machineries. It forms repressive complexes with methyl-CpG-binding protein MBD1 and the histone methyltransferase SETDB1, which catalyzes trimethylation of histone H3 at lysine 9 (H3K9me3). This activity leads to chromatin compaction and transcriptional silencing of target genes. Upstream regulators include the transcription factor ATF7 and SP1, while interacting partners also encompass RB1 and CAF-1. Through these interactions, ATF7IP mediates gene repression in processes such as stem cell pluripotency maintenance and epigenetic inheritance.
In the HeLa cell context, ablation of ATF7IP disrupts key epigenetic silencing networks. Given the role of aberrant DNA methylation and histone modifications in cervical cancer progression, this model is particularly relevant for dissecting how ATF7IP contributes to oncogenic gene expression programs. HPV-18 oncoproteins are known to interact with host epigenetic regulators, potentially intersecting with ATF7IP-associated complexes, thereby providing a platform to study viral-host interplay in chromatin remodeling and tumorigenesis.
Research applications of this product include Western blotting for ATF7IP and H3K9me3 levels, chromatin immunoprecipitation coupled with quantitative PCR (ChIP-qPCR) to map ATF7IP and histone marks at endogenous loci, and RNA sequencing to capture global transcriptomic changes upon ATF7IP disruption. Co-immunoprecipitation assays further allow investigation of interactions with MBD1 and SETDB1, while immunofluorescence enables subcellular localization studies. In addition, cell proliferation and apoptosis assays provide functional readouts in cancer-relevant contexts. For further details or to inquire about this product, please contact Ascent Research.
