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Cat. No. ARG38904

DLG5 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DLG5 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited cell population with disrupted DLG5, a scaffold protein linking cell polarity to Hippo and Wnt signaling. In HeLa cervical adenocarcinoma cells, which feature HPV18-driven p53 degradation, DLG5 knockout impairs junctional complexes and alters YAP/TAZ and CTNNB1 activity. This model supports studies on polarity-dependent tumor mechanisms, Hippo pathway regulation, and drug sensitivity. Representative assays include Western blotting, immunofluorescence, co-immunoprecipitation, and cell migration. It is a versatile tool for cancer and signaling research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    DLG5

    Gene Identifier

    NCBI Gene ID 9231

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 DLG5 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human DLG5 gene in HeLa cells. This loss-of-function model enables investigation of DLG5-dependent mechanisms in an immortalized, epithelial background. The polyclonal nature reflects diverse editing outcomes across the cell pool, offering a robust system for studying gene disruption effects without single-cell cloning bias.

HeLa cells, derived from a cervical adenocarcinoma, are widely used as an epithelial cancer model. They harbor integrated HPV18 sequences that produce the E6 oncoprotein, which targets p53 for degradation, thereby impairing cell cycle control and apoptosis. This immortalized line provides a consistent genetic background for studying cancer-related pathways and epithelial biology.

DLG5 encodes a scaffold protein essential for cell polarity and tight junction assembly. It functions downstream of PRKCA and ROCK kinases and Wnt ligands, forming complexes with PARD3, AMOT, and CTNNB1. DLG5 modulates Hippo signaling by influencing YAP/TAZ localization, and interacts with CTNNB1 to fine-tune Wnt transcriptional responses via TCF/LEF factors. Knockout of DLG5 disrupts these interactions, leading to altered Hippo pathway activity and compromised tight junction integrity.

In the HeLa background, loss of DLG5 removes a key polarity determinant while p53 remains inactivated, creating a model to dissect polarity-dependent tumor suppressive mechanisms independent of p53. The knockout cells exhibit diminished junctional scaffolding, potentially affecting YAP/TAZ and CTNNB1 signaling. This enables study of how DLG5 orchestrates crosstalk between the Hippo and Wnt pathways in an oncogenic context.

This polyclonal knockout population is suitable for assays including Western blotting, immunofluorescence, co-immunoprecipitation, migration, and proliferation studies. Applications include investigating cancer cell polarity, Hippo pathway regulation, and drug sensitivity testing. The cells provide a versatile tool for functional genomics and signaling interrogation. For more information, please contact Ascent Research.

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