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Cat. No. ARG37562

ATOH8 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The ATOH8 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population derived from HeLa cervical adenocarcinoma cells (HPV18-positive), serving as a loss-of-function model for the bHLH transcription factor ATOH8. ATOH8 mediates TGF-??/BMP signaling, interacting with SMAD1/2/3 and TCF3 to repress ID1/ID3 and promote CDH1 (E-cadherin), thereby regulating cell differentiation, proliferation, and epithelial-mesenchymal transition. This model is ideal for studying tumor suppression and EMT in cervical cancer research. Applications include western blot analysis of ATOH8 and pathway targets, RT-qPCR for ID1/ID3/CDH1, ChIP assays, and functional migration/invasion experiments, supporting drug discovery and basic cancer biology.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    ATOH8

    Gene Identifier

    NCBI Gene ID 84913

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The ATOH8 Knockout HeLa Polyclonal Cells consist of a CRISPR/Cas9-edited heterogeneous HeLa cell population carrying targeted disruption of the ATOH8 gene. As a polyclonal knockout product, this model provides a loss-of-function tool that eliminates functional ATOH8 protein while retaining population-level genetic diversity, thus minimizing clonal selection artifacts. It is designed for robust investigation of ATOH8??s role in signaling networks and cellular processes.

The parental HeLa cell line originates from a human cervical adenocarcinoma and is positive for HPV18 sequences, serving as a staple epithelial cancer model. HeLa cells recapitulate key aspects of cervical carcinogenesis, including aberrant signaling and HPV-oncoprotein-driven transformation. Their high proliferation rate and ease of genetic manipulation render them an ideal background for generating knockout models to probe tumor suppressor gene function.

ATOH8 (atonal bHLH transcription factor 8) is a key downstream mediator of TGF-?? and BMP signaling. Upon pathway activation, TGFBR1 phosphorylates SMAD2/3, which partner with SMAD4 and translocate to the nucleus to induce ATOH8 expression. ATOH8 subsequently forms transcriptional complexes with SMAD1, SMAD2/3, and the E-protein TCF3/E47. These complexes directly repress the pro-proliferative ID1 and ID3 genes while promoting the epithelial marker CDH1 (E-cadherin), thereby suppressing EMT and cell proliferation. Through this regulatory axis, ATOH8 acts as a tumor suppressor in multiple tissues, including the cervix.

In the context of HeLa cervical carcinoma cells, ATOH8 deficiency is predicted to exacerbate malignant features such as increased proliferation, motility, and mesenchymal transition. As HeLa cells already exhibit dysregulated TGF-??/BMP pathways due to HPV18 oncogenes, the ATOH8 knockout provides a specific model to assess how loss of this transcription factor contributes to cervical cancer progression. The polyclonal nature of the product allows researchers to evaluate the collective phenotypic impact without the biases of single-cell clones, making it especially useful for studying heterogeneous tumors.

This knockout cell population is suited for diverse investigations, including cancer biology (EMT, metastasis), neurodevelopment (bHLH factor function), and drug discovery screens targeting TGF-??/BMP signaling. Typical experimental readouts include western blotting for ATOH8 and pathway targets, RT-qPCR for ID1, ID3, and CDH1 transcript levels, and chromatin immunoprecipitation to validate ATOH8 binding. Functional assays such as wound healing, transwell migration, and invasion quantify motility changes, while immunofluorescence enables co-localization studies with SMAD partners. For further information or to explore custom cell engineering services, please contact Ascent Research.

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