The EEF1D Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the murine MES-OV ovarian surface epithelial cell line. This product features targeted disruption of the Eef1d gene, which encodes the delta subunit of elongation factor-1, resulting in a heterogeneous pool of cells with loss-of-function alleles. The polyclonal format provides a robust model for studying gene function while minimizing clonal artifacts, offering a versatile tool for translational research in cancer biology.
The MES-OV cell line is a spontaneously immortalized murine ovarian surface epithelial cell model that recapitulates key characteristics of the ovarian surface epithelium, the tissue of origin for many epithelial ovarian cancers. These cells provide a physiologically relevant background for investigating molecular mechanisms underlying ovarian carcinogenesis, including transformation, proliferation, and signaling pathway alterations.
EEF1D encodes the delta subunit of the elongation factor-1 complex, which is essential for translation elongation by catalyzing guanine nucleotide exchange on eEF1A, enabling the recycling of eEF1A for consecutive rounds of aminoacyl-tRNA delivery to the ribosome. EEF1D activity is regulated by the mTOR signaling pathway, growth factor signaling, and nutrient availability, positioning it as a critical nexus between anabolic signals and protein synthesis. It interacts closely with EEF1A, EEF1B2, EEF1G, ribosomal subunits, and aminoacyl-tRNA to facilitate efficient polypeptide elongation. Dysregulation of this complex can impact global protein synthesis and expression of proliferation-related proteins, linking EEF1D to cell growth and stress adaptation.
In MES-OV cells, EEF1D knockout disrupts the elongation factor-1 complex dynamics, leading to impaired translation elongation and consequent reduction in protein synthesis. Given the association of ovarian surface epithelial cells with ovarian carcinogenesis, this model enables dissection of how translational control contributes to malignant transformation and tumor progression. The interplay between EEF1D and the mTOR signaling cascade, a frequently hyperactivated pathway in epithelial cancers, makes this knockout system particularly relevant for exploring therapeutic vulnerabilities in ovarian cancer.
These polyclonal knockout cells are suitable for a wide range of investigations, including the assessment of translation regulation via polysome profiling, western blotting for elongation factor expression, and functional assays such as MTT, colony formation, and BrdU incorporation to evaluate cell proliferation and viability. They facilitate RNA-seq and proteomic analyses to uncover global changes in gene and protein expression upon EEF1D loss. Moreover, the model supports drug dose-response studies and synthetic lethality screens to identify compounds that selectively target cells with compromised translational machinery. For further details or custom modifications, please contact Ascent Research.
