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Cat. No. ARG40860

EHMT1 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The EHMT1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human ovarian clear cell carcinoma cell line MES-OV. EHMT1 is a histone H3K9 methyltransferase that functions in complex with EHMT2 and REST to repress transcription of targets such as CDKN1A and neuronal genes. This knockout model enables investigation of epigenetic regulation in ovarian cancer, supporting histone methyltransferase inhibitor testing, gene expression analysis via RT-qPCR, and assessment of H3K9 methylation by western blotting and ChIP. The polyclonal format provides a heterogeneous population for robust functional studies.

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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

    EHMT1

    Gene Identifier

    NCBI Gene ID 79813

    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 CRISPR/Cas9-edited EHMT1 Knockout MES-OV Polyclonal Cells provide a pooled population of MES-OV cells carrying targeted disruption of the EHMT1 gene. This polyclonal knockout model is designed for studying EHMT1 loss-of-function in the context of ovarian clear cell carcinoma, without clonal selection. The knockout cell population facilitates investigation of epigenetic regulation and transcriptional repression mechanisms dependent on EHMT1 activity.

MES-OV is a human ovarian clear cell carcinoma cell line, derived from patient tumor tissue and widely used as a model for ovarian clear cell adenocarcinoma. This adherent epithelial line retains key characteristics of the primary cancer, including relevant genetic alterations and growth properties. It is particularly valuable for preclinical studies of ovarian cancer biology and for testing therapeutic interventions targeting epigenetic regulators.

EHMT1 encodes a histone lysine methyltransferase that specifically catalyzes mono- and dimethylation of histone H3 at lysine 9 (H3K9me1/2), marks associated with transcriptional silencing and heterochromatin formation. EHMT1 functions in obligate complexes with its homolog EHMT2/G9a and is recruited to chromatin by transcription factors such as REST, which silences neuronal genes (e.g., BDNF, SYN1) in non-neuronal tissues. The enzyme also interacts with HP1 proteins, MPP8, and chromatin remodeling factors to maintain repressive chromatin states. EHMT1 directly regulates the tumor suppressor CDKN1A and operates within a pathway involving REST, CoREST, and H3K9 methylation to control gene expression programs.

In ovarian clear cell carcinoma cells, EHMT1-mediated H3K9 methylation may contribute to the epigenetic silencing of tumor suppressor genes and maintenance of the malignant phenotype. Disruption of EHMT1 in the MES-OV background allows researchers to assess its role in cancer cell proliferation, differentiation, and response to epigenetic therapies. The polyclonal knockout population offers a convenient system for evaluating the functional consequences of EHMT1 loss without the artifacts of clonal selection, providing a more representative model of heterogeneous tumor cell populations.

Typical research applications include western blotting for H3K9me1/2 levels, RT-qPCR analysis of downstream targets such as CDKN1A and neuronal genes, ChIP-qPCR to measure H3K9me2 enrichment at specific loci, and immunofluorescence for HP1 foci formation as a readout of heterochromatin integrity. The cells are also suitable for functional genomics screens, cell proliferation and drug sensitivity assays with EHMT inhibitors, and mechanistic studies of REST and EHMT2 interaction networks in ovarian cancer. For further details, please contact Ascent Research.

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