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Cat. No. ARG38897

DLG3 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DLG3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human cervical carcinoma HeLa cell line, featuring targeted disruption of the DLG3 gene encoding the SAP102 scaffold protein. SAP102 organizes postsynaptic density complexes and links NMDA receptor trafficking to Wnt/??-catenin signaling through interactions with APC, PTEN, and ??-catenin. This model enables investigation of DLG3's non-neuronal roles in cancer-relevant processes such as cell adhesion, polarity, and proliferation. Applications include co-immunoprecipitation, Wnt reporter assays, migration and proliferation analyses, and RT-qPCR profiling of downstream targets.

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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

    DLG3

    Gene Identifier

    NCBI Gene ID 1741

    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 DLG3 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of HeLa cells with targeted disruption of the human DLG3 gene, which encodes the SAP102 scaffolding protein. This polyclonal format consists of a heterogeneous pool of gene-edited cells, suitable for loss-of-function studies without clonal isolation. The CRISPR/Cas9-mediated gene disruption ablates SAP102 expression, enabling investigation of its roles in signal transduction and cellular organization.

HeLa cells are an extensively characterized human cervical carcinoma line derived from HPV18-positive adenocarcinoma, featuring inactivation of the p53 and Rb tumor suppressors, high proliferation rates, and an aneuploid karyotype. Their epithelial origin and robust growth characteristics make them a standard model for cancer biology, cell signaling, and cytoskeletal studies, providing a relevant context for assessing the non-neuronal functions of the DLG3-encoded scaffold protein.

As a MAGUK family member, SAP102 organizes postsynaptic density-like complexes by scaffolding NMDA receptor subunits (GluN1, GluN2), adaptor proteins (PSD-95, GKAP, Shank), and tumor suppressors APC and PTEN. It is activated by NMDA receptor signaling and phosphorylated by CaMKII, Src kinases, and PKC, and mediates downstream Wnt/??-catenin pathway activation through ??-catenin stabilization and TCF/LEF transcriptional regulation. SAP102 also interacts with Kir2.3 channels and cytoskeletal components (actin, spectrin), thereby coupling synaptic-like signaling to cell polarity and adhesion.

In the HeLa epithelial background, DLG3 knockout disrupts the SAP102-anchored network that links Wnt/??-catenin signaling, cell adhesion, and polarity. Since SAP102 associates with the tumor suppressors APC and PTEN??both commonly dysregulated in cervical cancers??its loss may alter ??-catenin-dependent transcription, cytoskeletal dynamics, and migratory behavior. This model thus enables dissection of how a synaptic scaffold protein contributes to cancer-relevant processes independently of neuronal context.

The DLG3 knockout HeLa cells support applications including Western blot confirmation of protein loss, co-immunoprecipitation of interacting partners, immunofluorescence localization studies, Wnt reporter assays to measure ??-catenin activity, and functional assays for proliferation and migration. RT-qPCR can monitor transcriptional changes in targets like ??-catenin and TCF/LEF. These cells are suited for screening compounds that modulate SAP102-mediated pathways and for comparative studies of MAGUK family function in cancer cell biology. For further details, contact Ascent Research.

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