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Cat. No. ARG38881

DLG1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

DLG1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the tumor suppressor DLG1 in HeLa human cervical epithelial cells. DLG1 scaffolds tight junction and polarity complexes, and its loss, as induced by HPV E6, potentiates Wnt/??-catenin and Hippo signaling, interacting with APC, PTEN, and ??-catenin. This model is ideal for studying cell polarity, tight junction biology, HPV-mediated oncogenesis, and tumor suppression. Applications include western blotting, immunofluorescence, TEER measurement, and migration/invasion assays, providing a versatile tool for cancer and epithelial biology 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

    DLG1

    Gene Identifier

    NCBI Gene ID 1739

    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

DLG1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting DLG1 in the HeLa human cervical epithelial line. This loss-of-function model, generated via CRISPR/Cas9-mediated gene disruption, maintains allelic diversity suitable for population-level phenotypic studies without clonal selection bias. It serves as a robust platform for investigating DLG1-dependent processes, including cell polarity, tight junction biology, and tumor suppression.

The HeLa cell line originates from a cervical adenocarcinoma of Henrietta Lacks. HPV18-positive, these cells express viral oncoproteins E6 and E7, driving transformation. Their epithelial morphology and extensive characterization make HeLa cells a staple in cancer biology and signal transduction research, providing a relevant background for examining tumor suppressor genes like DLG1 in oncogenic contexts.

DLG1 is a MAGUK scaffold protein critical for tight junction assembly and cell polarity. It interacts with APC, PTEN, LIN7, and CASK, coupling the actin cytoskeleton to junctional complexes. DLG1 participates in the Hippo pathway by modulating MST1/2, LATS1/2, and YAP/TAZ, and in the Wnt pathway by scaffolding APC and ??-catenin to restrain ??-catenin transcriptional activity. The HPV E6 oncoprotein targets DLG1 for degradation, linking viral oncogenesis to polarity loss. Thus, DLG1 disruption compromises tight junction integrity and deregulates Hippo and Wnt/??-catenin signaling, potentially enhancing PI3K/AKT pathway activity.

In HeLa cells, DLG1 knockout recapitulates E6-mediated degradation, driving HPV-associated carcinogenesis. Loss of DLG1 disrupts epithelial barrier function, promotes invasive behavior, and activates proliferative signals. This model enables dissection of DLG1’s tumor suppressor role in an HPV-positive background, facilitating studies on migration, invasion, and transformation. The polyclonal format allows examination of heterogeneous responses and compensatory mechanisms following gene disruption.

Research applications include western blotting and immunofluorescence for protein analysis, co-immunoprecipitation for interaction networks, and transwell assays for migration/invasion. Barrier function can be assessed via TEER measurement, and pathway activities via luciferase reporters for Wnt and Hippo signaling. The cells are relevant for HPV oncogenesis, neurodevelopmental disorder models, and cell polarity studies. For more information or custom requests, contact Ascent Research.

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