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Cat. No. ARG40809

EHD3 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The EHD3 Knockout MES-OV Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the MES-OV human ovarian carcinoma cell line, with targeted disruption of the EHD3 gene. This model enables loss-of-function studies of EHD3, an ATPase critical for endocytic recycling of key receptors such as EGFR and transferrin receptor. EHD3 knockout is particularly suited for investigating receptor trafficking, integrin-mediated migration, and oncogenic signaling in ovarian cancer. Applications range from basic endocytosis research to drug discovery, utilizing assays like transferrin uptake, immunofluorescence, and proliferation measurements.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    MES-OV

    Sex of Donor

    Female

    Age

    53 years

    Derived From Site

    Ascites

    Gene Name

    EHD3

    Gene Identifier

    NCBI Gene ID 30845

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 EHD3 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-mediated gene disruption model, offering a polyclonal knockout cell population derived from the MES-OV human ovarian carcinoma cell line. This polyclonal format avoids biases associated with single-cell cloning, providing a diverse pool of cells with EHD3 loss-of-function for robust and reproducible studies of endocytic trafficking pathways.

The MES-OV cell line is an established model of human ovarian carcinoma, retaining key oncogenic signaling networks and epithelial characteristics relevant to ovarian cancer biology. Its use as the host for EHD3 knockout enables investigation of endosomal recycling mechanisms in the context of ovarian cancer pathogenesis, including altered receptor trafficking and cell migration typically observed in malignant progression.

EHD3 encodes an ATPase that functions as a key regulator of endocytic recycling, controlling the trafficking of multiple receptors including EGFR, transferrin receptor, integrin ??5??1, and the cardiac sodium channel NaV1.5. EHD3 interacts with endosomal machinery components such as Rab11a, Rab11-FIP2, and Arf6, as well as syndapin, amphiphysin, and ankyrin-G. Upstream regulators include EGF, DNMT1, and HIF1A, while downstream consequences of EHD3 activity involve modulation of EGFR surface expression, transferrin receptor recycling, and integrin-dependent cell migration and proliferation. Disruption of EHD3 impairs these recycling routes, leading to altered signaling outputs and cellular responses.

In the MES-OV ovarian cancer background, EHD3 knockout is expected to perturb EGFR and integrin trafficking, thereby affecting key oncogenic processes such as proliferation, migration, and invasion. This model enables the dissection of endosomal recycling contributions to ovarian cancer cell behavior and may help identify therapeutic vulnerabilities linked to receptor trafficking defects. It also serves as a platform to study the intersection of endocytosis and oncogenic signaling in a disease-relevant cellular environment.

Typical applications include endocytosis and receptor trafficking studies, functional analyses of EGFR and integrin dynamics, and drug discovery efforts targeting trafficking-related pathways. Experimental readouts can utilize transferrin uptake assays, immunofluorescence and flow cytometry for surface receptor quantification, western blotting for protein expression, and functional assays such as transwell migration and proliferation measurements. This polyclonal knockout population is suitable for both mechanistic investigations and high-throughput screening campaigns. For additional information, please contact Ascent Research.

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