The ANKRD17 polyclonal knockout HeLa cells are a CRISPR/Cas9-edited cell population with targeted disruption of the ANKRD17 gene, providing a loss-of-function model for functional studies. This polyclonal product format comprises a heterogeneous pool of cells harboring gene edits at the ANKRD17 locus, generated without single-cell cloning to maintain population diversity while achieving robust target-gene ablation. The knockout model is suitable for investigating the scaffold protein’s roles across various experimental contexts.
The host cell line, HeLa, is an immortalized human cervical epithelial cell line originally derived from an HPV18-positive cervical adenocarcinoma of an African American female. HeLa cells exhibit robust proliferation and are extensively characterized for studying cancer cell biology, signaling pathways, and cytoskeletal organization. Their transformed phenotype and epithelial origin make them an ideal platform for examining molecular mechanisms underlying cervical cancer progression, cell adhesion, and migration.
ANKRD17 encodes an ankyrin repeat-containing scaffold protein that physically bridges the actin and microtubule cytoskeletons by interacting with ACTB and TUBA1A. It functions as a signaling node at the intersection of Wnt/??-catenin and Hippo pathways. ANKRD17 is regulated upstream by the ??-catenin/TCF complex, TGF-??/SMAD signaling, and focal adhesion kinase (FAK). It directly interacts with CTNNB1, TCF7L2, YAP1, PTPN11, SMAD2, and SMAD3, modulating transcriptional outputs. Downstream, ANKRD17 promotes actin polymerization, microtubule stability, cell migration, and Wnt target gene expression, while also influencing YAP/TAZ-mediated transcription.
In HeLa cells, ANKRD17 knockout disrupts cytoskeletal architecture, impairs cell adhesion and migration, and perturbs Wnt/??-catenin and Hippo signaling crosstalk. This leads to altered transcriptional responses driven by ??-catenin and YAP, which are critical for epithelial-mesenchymal transition and tumor invasion. The polyclonal knockout model is particularly relevant for dissecting the signaling networks that drive cervical cancer cell motility and for modeling neurodevelopmental disorders associated with ANKRD17 mutations, such as intellectual disability and autism spectrum disorder.
These ANKRD17 knockout cells support diverse assays including western blotting for ANKRD17, immunofluorescence to assess actin and microtubule organization, wound healing and transwell invasion assays for migration and invasion, co-immunoprecipitation to map interactions with CTNNB1, YAP1, or SMAD2, RT-qPCR for Wnt target genes, and TCF/LEF luciferase reporter assays. Applications encompass cytoskeletal dynamics, Wnt-Hippo crosstalk, cervical cancer invasion, neurodevelopmental disease modeling, and drug discovery targeting cytoskeletal scaffolds. For further information or to inquire about this knockout cell product, please contact Ascent Research.
