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Cat. No. ARG35759

C12orf10 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

The MYG1 Knockout A2780 Polyclonal Cells provide a heterogeneous pool of CRISPR/Cas9-edited A2780 ovarian carcinoma cells with disruption of the nuclear gene MYG1. MYG1 encodes a mitochondrial 3'-5' exonuclease essential for mitochondrial ribosome assembly, translation fidelity, and expression of mtDNA-encoded OXPHOS subunits such as MT-CO1 and MT-ND1. This polyclonal knockout pool enables investigation of mitochondrial translation in ovarian cancer, metabolic reprogramming, and cisplatin sensitivity. MYG1 is regulated by NRF1 and PGC-1??, interacts with MRPL2, MRPL44, and mitochondrial RNA granule components, and serves as a valuable tool for studying mitochondrial-nuclear crosstalk and mitochondrial disease mechanisms.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A2780

    Sex of Donor

    Female

    Age

    Unknown

    Derived From Site

    In situ; Ovary

    Gene Name

    C12orf10

    Gene Identifier

    NCBI Gene ID 60314

    Morphology

    Epithelial-like

    Growth Mode

    Adherent and suspension

    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 MYG1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted disruption of the MYG1 gene, designed for studying loss-of-function effects in mitochondrial biology and ovarian cancer research. The polyclonal format eliminates the need for single-cell cloning and preserves population diversity, making it suitable for pooled functional screens or bulk biochemical assays where clonal artifacts are undesirable.

The A2780 cell line is a well-characterized model of epithelial ovarian cancer, established from an untreated endometrioid adenocarcinoma. With a near-diploid karyotype and retained cisplatin sensitivity, it is widely used to study drug resistance and metabolic adaptation. Its epithelial origin and stable genome provide a robust platform for probing mitochondrial gene disruptions in cancer.

MYG1 encodes a mitochondrial 3′-5′ exoribonuclease essential for RNA processing and ribosome assembly. It is regulated by NRF1 and PGC-1?? and modulated by mitochondrial stress signals. MYG1 interacts with large-subunit proteins MRPL2 and MRPL44, GTPBP10, and RNA granule components PNPase and GRSF1 to facilitate mitochondrial transcript maturation and incorporation of MRPLs and MRPSs. This activity directly governs mtDNA-encoded OXPHOS subunits MT-CO1 and MT-ND1, linking ribosome biogenesis to the oxidative phosphorylation system.

Disruption of MYG1 in these cisplatin-sensitive ovarian cancer cells provides a physiologically relevant system to dissect the contribution of mitochondrial translation and oxidative phosphorylation to cancer cell fitness and drug response. Ovarian cancer cells are known to undergo metabolic rewiring, and mitochondrial defects can modulate sensitivity to platinum-based chemotherapies. This polyclonal knockout pool enables direct comparison with wild-type A2780 cells, facilitating the study of mitochondrial-nuclear crosstalk and identification of metabolic vulnerabilities that may be exploited therapeutically.

The MYG1 polyclonal knockout cells are suitable for a broad range of functional assays. Researchers can assess OXPHOS complex expression by western blotting, measure de novo mitochondrial protein synthesis via pulse-chase labeling, and profile oxygen consumption using Seahorse respirometry. Additional applications include cell viability assays under cisplatin exposure, mtDNA copy number quantification by qPCR, immunofluorescence staining for mitochondrial markers, and RNA immunoprecipitation to detect MYG1-bound transcripts. For further technical information, please contact Ascent Research.

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