The ANKMY2 Knouckout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product provides a loss-of-function model for studying the ankyrin repeat and MYND domain-containing protein ANKMY2, a putative transcriptional coregulator. The polyclonal knockout pool contains a heterogeneous mixture of cells harboring various CRISPR/Cas9-mediated disruptions in the ANKMY2 gene, enabling robust assessment of gene function without clonal artifacts. The cells are suitable for a range of biochemical and cell-based assays and are designed for use in chromatin biology and cancer research.
The HT29 host cell line was originally isolated from a primary colorectal adenocarcinoma and is widely used as a model for intestinal epithelial biology and colorectal cancer. These adherent epithelial cells harbor characteristic colon cancer mutations, including in the APC, TP53, and KRAS genes, and maintain critical features of the disease, such as dysregulated Wnt signaling, altered apoptosis, and defective differentiation. HT29 cells are a well-established platform for investigating mechanisms of colon carcinogenesis and for evaluating therapeutic interventions, making them a clinically relevant background for studying the role of chromatin regulators like ANKMY2 in malignancy.
ANKMY2 encodes an ankyrin repeat and MYND domain-containing protein that functions as a putative transcriptional coregulator within the SRCAP chromatin remodeling complex. This protein is thought to regulate the deposition of the histone variant H2A.Z, thereby modulating chromatin structure and gene expression. ANKMY2 interacts with key components of the SRCAP complex, including SRCAP, RUVBL1, and RUVBL2, and is associated with histone deacetylases and other corepressor proteins. While upstream regulators remain largely uncharacterized, ANKMY2 may be influenced by Wnt/??-catenin signaling, and it transcriptionally regulates downstream targets such as the cell cycle promoter CCND1, the pro-apoptotic factor BAX, and the intestinal differentiation marker VIL1. Thus, ANKMY2 occupies a node linking chromatin remodeling to transcriptional programs controlling proliferation, apoptosis, and differentiation.
In the HT29 colorectal adenocarcinoma context, ANKMY2 knockout provides a powerful tool for dissecting the role of H2A.Z dynamics and SRCAP complex function in colon cancer biology. Because HT29 cells express oncogenic signaling networks driven by APC and KRAS mutations, disruption of ANKMY2 may reveal how chromatin-level regulation intersects with these pathways to sustain tumorigenic phenotypes. This knockout model allows researchers to examine changes in H2A.Z localization, global transcriptome remodeling, and alterations in cell fate decisions, thereby offering insights into the contribution of ANKMY2 to colorectal cancer progression and potential therapeutic vulnerabilities associated with chromatin dysregulation.
The ANKMY2 Knouckout HT29 Polyclonal Cells are ideally suited for a variety of downstream applications, including targeted gene expression analysis by RT-qPCR or RNA-seq, chromatin immunoprecipitation (ChIP) to map H2A.Z occupancy changes, and phenotypic assays such as proliferation, apoptosis (Annexin V staining), and migration/invasion (transwell) studies. Additional experiments may involve Western blotting to confirm ANKMY2 protein loss and immunofluorescence to examine subcellular localization of interacting factors. Researchers can also use this model to screen for synthetic lethal interactions or drug sensitivities that arise upon ANKMY2 disruption. For further technical inquiries or protocol support, customers are encouraged to contact Ascent Research.
