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Cat. No. ARG40865

EHMT1 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

The EHMT1 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Huh-7 hepatocellular carcinoma cell line, enabling loss-of-function studies of the histone methyltransferase EHMT1. EHMT1 deposits H3K9me1/me2 marks and represses transcription of tumor suppressors such as CDH1 and CDKN1A, often downstream of ATF4 and MYC. This model is ideal for investigating epigenetic silencing in liver cancer, performing ChIP-qPCR for H3K9me2, RNA-seq, drug sensitivity assays, and examining reactivation of silenced genes. The polyclonal format provides a robust, heterogeneous knockout background for reproducible functional analyses.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    EHMT1

    Gene Identifier

    NCBI Gene ID 79813

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 EHMT1 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for functional studies of EHMT1. Derived from the Huh-7 hepatocellular carcinoma line, these cells feature targeted disruption of the EHMT1 gene via CRISPR/Cas9, providing a heterogeneous loss-of-function model without single-cell cloning. This polyclonal product enables robust analysis of EHMT1-dependent epigenetic pathways in liver cancer.

Huh-7 is an epithelial cell line established from a liver tumor of a 57-year-old Japanese male in 1982. It serves as a widely used model for hepatocellular carcinoma and liver metabolism studies, retaining key hepatic features and tumorigenic properties ideal for gene-editing applications.

EHMT1 encodes a histone H3K9 methyltransferase that generates H3K9me1/me2 marks, leading to chromatin compaction and transcriptional repression. It functions as a heterodimer with EHMT2 and interacts with corepressor complexes containing CtBP, WIZ, and histone deacetylases, recruiting HP1 proteins to methylated nucleosomes. In HCC, EHMT1 is upregulated by ATF4 and MYC, causing silencing of tumor suppressors such as CDH1 (E-cadherin) and CDKN1A (p21). CRISPR-mediated knockout relieves this repression, potentially reactivating these genes and attenuating oncogenic phenotypes.

This polyclonal knockout model enables investigation of H3K9 methylation dynamics in HCC without clonal biases. By disrupting EHMT1-mediated silencing, researchers can examine the interplay between histone methylation and DNA methylation (via DNMT1) in maintaining a repressive chromatin state. The heterogeneous population reflects average gene-disruption effects, making it suitable for studying tumor-suppressor reactivation and pathway crosstalk in a liver cancer context.

Typical applications include RNA-seq for transcriptome profiling, ChIP-qPCR for H3K9me2 at target promoters (e.g., CDH1, CDKN1A), western blotting for EHMT1 protein verification, and functional assays for proliferation, apoptosis, and drug sensitivity. These cells are also useful for screening EHMT1 inhibitors and validating downstream effectors. For further details, contact Ascent Research.

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