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Cat. No. ARG38920

DLGAP4 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The DLGAP4 Knockout MES-OV Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of MES-OV mouse ovarian surface epithelial cells with disrupted SAPAP4 (DLGAP4) expression. DLGAP4 encodes a scaffolding protein that links DLG1/DLG4 MAGUKs to the actin cytoskeleton and ??-catenin at cell junctions, integrating Wnt, Hippo, and integrin signaling to maintain epithelial polarity and homeostasis. This knockout model enables detailed investigation of how DLGAP4 loss compromises junctional integrity, alters YAP/TAZ and Wnt pathway activity, and contributes to ovarian epithelial disorganization. It is ideal for functional studies, EMT assays, drug screening, and mechanistic exploration of ovarian cancer initiation in a non-tumorigenic background.

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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

    DLGAP4

    Gene Identifier

    NCBI Gene ID 22839

    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 DLGAP4 Knockout MES-OV Polyclonal Cells product supplies a CRISPR/Cas9-edited polyclonal knockout cell population in which the gene encoding SAPAP4 (DLGAP4) has been disrupted in the MES-OV mouse ovarian surface epithelial cell line. This polyclonal pool contains a mixed population of edited cells, providing a loss-of-function model for studying DLGAP4-dependent processes in an epithelial context without clonal selection artifacts. The knockout population is suited for experiments requiring bulk functional analysis of DLGAP4 ablation, such as signaling pathway interrogation and tumorigenicity assays.

The MES-OV cell line is a spontaneously immortalized mouse ovarian surface epithelial line that maintains a non-tumorigenic phenotype. It recapitulates key features of ovarian surface epithelium, which undergoes cyclic wound repair and proliferation during ovulation, providing a relevant model for studying early events in ovarian neoplastic transformation.

DLGAP4 encodes SAPAP4, a scaffold protein that couples DLG/MAGUK family members (e.g., DLG1/SAP97, DLG4/PSD-95) to the actin cytoskeleton at epithelial junctions. SAPAP4 also recruits SHANK proteins and ??-catenin into junctional complexes, thereby organizing signaling centers. Its expression is regulated by Wnt ligands, EGF/EGFR, TGF-??, and integrin-mediated adhesion, which trigger downstream effectors including JNK/MAPK signaling and the stabilization of tight junction (claudin, occludin) and adherens junction (E-cadherin/??-catenin) components. Importantly, DLGAP4 intersects with the Hippo pathway by influencing the localization and activity of Scribble, LATS1/2, and YAP/TAZ, linking cell?Ccell adhesion to growth control.

Disruption of DLGAP4 in MES-OV cells likely compromises junctional integrity and polarity by uncoupling MAGUK proteins from the cytoskeleton, impairing Hippo and Wnt/??-catenin signaling. This leads to deregulated YAP/TAZ and ??-catenin activity, mimicking early tumorigenic changes. The non-tumorigenic nature of the line allows investigation of cooperative oncogenic events required for full transformation.

This DLGAP4 polyclonal knockout cell population is well-suited for a broad range of advanced research applications, including quantitative analysis of DLGAP4 expression by Western blotting and RT-qPCR, visualization of junctional markers (E-cadherin, ZO-1) via immunofluorescence, and functional assays such as cell adhesion, transwell migration/invasion, and proliferation measurements. Additionally, it supports mechanistic studies of Hippo-Wnt crosstalk using phospho-YAP detection and Wnt reporter assays. Researchers investigating ovarian epithelial homeostasis, epithelial-to-mesenchymal transition (EMT), or screening adhesion-targeted therapeutics will find this model a powerful tool for elucidating DLGAP4??s role in normal and pathological states. For further information, please contact Ascent Research.

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