HES7 Knockout HeLa Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of HeLa cells featuring genetic disruption of the HES7 gene. This loss-of-function model was generated by CRISPR/Cas9-mediated gene editing, resulting in a heterogeneous pool of edited alleles that functionally abolish HES7 expression. The polyclonal format provides a robust system for studying HES7-dependent functions while minimizing clonal artifacts, making it well-suited for population-level assays and high-throughput screening applications.
The host HeLa cell line is an HPV-18 positive human cervical adenocarcinoma with an epithelial-like morphology. As one of the most widely used immortalized cell lines in biomedical research, HeLa cells provide a standardized and reproducible human cellular context for investigating gene function. Their robust growth properties and amenability to transfection and genetic manipulation make them an ideal platform for generating knockout models to dissect signaling pathways and cellular processes.
HES7 encodes a basic helix-loop-helix (bHLH) transcriptional repressor activated by Notch signaling. Upon Notch ligand?Creceptor engagement (DLL1/3/4?CNotch1/2), the NICD/RBP-J transcription complex induces HES7 expression. HES7 protein then represses its own promoter and those of LFNG and HES1, creating a negative feedback loop critical for oscillatory gene expression. HES7 mediates repression by interacting with TLE1-4/Groucho corepressors and E proteins (E12/E47), integrating with MAML and Hey family factors.
Disruption of HES7 in HeLa cells provides a tool for studying Notch-mediated oscillatory dynamics. Although HeLa cells do not undergo somitogenesis, they express Notch pathway components and support analysis of HES7??s auto-repressive function and target gene regulation. This model enables investigation of how HES7 loss affects downstream targets, protein interactions, and cellular responses to Notch activation. It also serves as an in vitro model for congenital vertebral segmentation defects like spondylocostal dysostosis.
The HES7 Knockout HeLa Polyclonal Cells are designed for functional characterization of HES7 in Notch signaling, including dissection of oscillatory feedback mechanisms and disease modeling for spondylocostal dysostosis. Key experimental approaches include RT-qPCR for oscillatory genes (HES7, LFNG, HES1), Western blotting for Notch pathway components, Notch luciferase reporter assays, co-immunoprecipitation with TLE corepressors, and immunofluorescence staining. Cellular proliferation (MTT) and apoptosis (Annexin V) assays enable assessment of HES7-dependent growth effects. This model is particularly suited for screening small molecules that modulate the segmentation clock. For additional technical information, please contact Ascent Research.
