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Cat. No. ARG37744

AS3MT Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

The AS3MT Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with disruption of the AS3MT gene in the HEK293T human embryonic kidney cell line. AS3MT catalyzes the S-adenosylmethionine-dependent methylation of arsenite to monomethylarsonic acid and dimethylarsinic acid, a critical detoxification pathway regulated by factors such as NRF2 and HIF1A. This knockout model enables investigation of arsenic metabolism, toxicity, and associated disease risks including cancer susceptibility and hepatotoxicity. Suitable for toxicology, pharmacogenomics, and environmental health research, these cells support assays like arsenic sensitivity testing and methylation activity measurements.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    AS3MT

    Gene Identifier

    NCBI Gene ID 57412

    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 AS3MT Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the AS3MT gene has been disrupted. This product provides researchers with a physiologically relevant loss-of-function model to investigate arsenic metabolism and detoxification. The polyclonal pool preserves heterogeneous editing events across the cell population, enabling robust phenotypic analysis without clonal selection biases.

These cells are derived from the extensively characterized HEK293T host line, a human embryonic kidney epithelial cell line expressing the SV40 large T-antigen. The HEK293T background is widely employed in biomedical research due to its high transfection efficiency and robust protein expression capabilities. Its epithelial origin makes it particularly suitable for studying xenobiotic metabolism and toxicological responses in a kidney-relevant context.

AS3MT encodes arsenic (+3 oxidation state) methyltransferase, which catalyzes the S-adenosylmethionine-dependent methylation of inorganic arsenite to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). This sequential biotransformation is the primary route for arsenic detoxification and facilitates excretion. AS3MT expression is regulated by stress-responsive transcription factors including NRF2, HIF1A, and AP-1, linking arsenic methylation to oxidative stress and cellular defense pathways. The enzyme??s activity directly influences the balance between toxic trivalent intermediates and excreted methylated products.

In the HEK293T cellular context, disruption of AS3MT creates a powerful system to dissect the molecular determinants of arsenic toxicity. Because these cells lack functional AS3MT, they are expected to exhibit reduced methylation capacity, leading to altered cellular sensitivity to arsenite and accumulation of inorganic arsenic species. This knockout model allows precise evaluation of how arsenic detoxification interfaces with pathways governing hepatotoxicity and cancer susceptibility, and can be used to identify compensatory mechanisms or modifier genes involved in arsenic-related pathologies.

The AS3MT Knockout HEK293T Polyclonal Cells are well-suited for toxicology, pharmacogenomics, cancer research, and environmental health investigations. Typical assays include arsenic sensitivity profiling, methylation activity measurements, MTT viability tests, and apoptosis analyses, complemented by Western blotting, RT-qPCR, and RNA-seq for molecular characterization. These polyclonal cells provide a critical platform for elucidating arsenic detoxification mechanisms and their disease relevance. For further details or assistance, contact Ascent Research.

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