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Cat. No. ARG39202

DNAJC13 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The DNAJC13 Knockout MES-OV Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal loss-of-function model in the ovarian clear cell carcinoma cell line MES-OV. DNAJC13 (RME-8) is a co-chaperone essential for endosomal sorting and retromer-mediated retrograde transport, interacting with the retromer complex, WASH complex, and SNX1/2. This knockout tool enables studies of cargo receptor trafficking (Sortilin, CI-MPR, EGFR), autophagy flux, and retromer function. Typical applications include Western blotting, immunofluorescence, transferrin recycling assays, and drug screening for neurodegenerative or cancer indications. Contact Ascent Research for more information.

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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

    DNAJC13

    Gene Identifier

    NCBI Gene ID 23317

    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 DNAJC13 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of MES-OV cells with disrupted DNAJC13 expression. Generated by CRISPR/Cas9-mediated gene disruption, this polyclonal knockout cell model enables loss-of-function studies without clonal selection artifacts. It provides a genetically defined platform for investigating DNAJC13-dependent endosomal trafficking and retromer biology.

These knockout cells are derived from the MES-OV human ovarian clear cell carcinoma cell line, an established epithelial ovarian cancer model. MES-OV cells retain characteristic features of ovarian clear cell carcinoma, including relevant oncogenic signaling networks and epithelial morphology. This cancer cell background offers a unique platform for studying how endosomal sorting and protein trafficking pathways intersect with tumor cell biology, drug response, and cellular stress mechanisms. The MES-OV host cells are widely employed in cancer research, providing a robust context for genetic perturbation studies aimed at dissecting membrane trafficking in malignancy.

DNAJC13, also known as RME-8, functions as a co-chaperone orchestrating endosomal protein sorting and retromer-mediated retrograde transport from endosomes to the trans-Golgi network. It acts downstream of PI(3)P and Hsc70, regulated by Rab GTPases, and interacts directly with the retromer complex (VPS35, VPS26, VPS29), the WASH complex, and SNX1/2. These interactions facilitate actin nucleation and cargo trafficking, governing recycling and degradation of transmembrane receptors. DNAJC13 controls retrograde transport of Sortilin, CI-MPR, and Wntless, and influences EGFR degradation, intersecting with growth factor signaling and autophagy.

In the MES-OV ovarian cancer context, DNAJC13 knockout disrupts the endosomal-lysosomal system, allowing exploration of how endosome dynamics influence tumor cell homeostasis. Although primarily associated with Parkinson disease and neurodegeneration, DNAJC13??s role in protein trafficking may affect cancer-relevant processes like receptor turnover, autophagy, and therapy response. This model enables interrogation of retromer-dependent transport contributions to ovarian cancer cell proliferation and survival, while also serving as an isogenic platform for studying neurodegeneration pathways in a non-neuronal background.

The DNAJC13 Knockout MES-OV Polyclonal Cells are suited for endosomal trafficking studies, retromer functional analysis, and autophagy research. Users can assess cargo receptor fate via EGFR degradation and transferrin recycling assays, examine retromer complex integrity by co-immunoprecipitation, and evaluate autophagy flux. Additional applications include immunofluorescence, flow cytometry for protein quantification, and high-content screening for trafficking modulators. This knockout model supports drug discovery targeting the endosomal pathway and provides a resource for Parkinson??s disease modeling. For additional information, please contact Ascent Research.

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