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Cat. No. ARG37399

HOXD9 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The HOXD9 Knockout HeLa Polyclonal Cells are CRISPR/Cas9-edited polyclonal knockout HeLa cells with targeted disruption of the HOXD9 gene. HOXD9 encodes a homeodomain transcription factor that interacts with PBX1 and MEIS1 to regulate developmental gene expression downstream of retinoic acid, FGF, SHH, and WNT pathways. Knockout of HOXD9 disrupts transcriptional programs governing epithelial differentiation and proliferation. This model is suited for investigating HOX gene regulatory networks, cervical cancer biology, and gene regulation. It enables western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, immunofluorescence, and functional assays including migration, invasion, and colony formation, supporting drug target identification and mechanistic studies in 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

    HOXD9

    Gene Identifier

    NCBI Gene ID 3235

    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 HOXD9 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, with targeted disruption of the HOXD9 gene. This loss-of-function model enables investigation of HOXD9-dependent transcriptional programs in a human epithelial cell background. The polyclonal format captures heterogeneous editing events across the population, providing a robust tool for studying gene function without clonal selection artifacts.

HeLa cells are an immortalized epithelial cell line originally isolated from cervical adenocarcinoma. They serve as a widely utilized model for cervical cancer research, offering well-characterized growth properties, high transfection efficiency, and compatibility with diverse functional assays. The HeLa background provides a relevant context for exploring HOXD9??s role in cervical carcinogenesis, given the gene??s implication in anterior-posterior patterning and tumor progression.

HOXD9 encodes a homeodomain transcription factor that operates within the HOX gene regulatory network, integrating signals such as retinoic acid, FGF, SHH, and WNT to orchestrate developmental gene expression. It forms heterodimeric complexes with PBX1 and MEIS1, and cooperates with PREP1 to regulate downstream targets including other HOX genes and cell adhesion molecules. Knockout of HOXD9 disrupts these transcriptional complexes and impairs differentiation and proliferation programs, providing a platform to dissect retinoic acid and WNT-dependent signaling. Representative pathway components affected by HOXD9 loss include retinoic acid receptors and HOXD9-PBX/MEIS transcriptional assemblies that control target gene expression.

In the HeLa context, HOXD9 knockout likely alters gene networks governing epithelial differentiation and malignancy. Given its role in limb development and cervical cancer, this model enables correlation of molecular changes with phenotypic outcomes such as altered migration, invasion, and colony formation. The disruption of HOXD9 expression in HeLa cells provides a controlled system to evaluate how anterior-posterior patterning cues intersect with oncogenic pathways, potentially revealing vulnerabilities in cervical and colorectal cancer models.

This knockout product supports diverse experimental workflows, including western blotting for protein expression analysis, RT-qPCR and RNA-seq for transcriptome profiling, and ChIP-qPCR to assess transcription factor occupancy at target loci. Functional studies can employ immunofluorescence, migration and invasion assays, and colony formation assays to characterize phenotypes associated with HOXD9 loss. The model is particularly suited for dissecting HOX gene regulatory networks, Wnt signaling, and retinoic acid signaling in cancer biology and gene regulation. For additional technical details or custom inquiries, please contact Ascent Research.

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