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Cat. No. ARG38815

DIXDC1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The DIXDC1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited ovarian cancer cell pool lacking DIXDC1, a scaffold protein that bridges DVL and AXIN to enhance Wnt/??-catenin signaling and drive expression of CCND1 and MYC. This model enables study of DIXDC1-dependent proliferation, migration, and cisplatin response. Typical assays include TOPFlash/FOPFlash reporter, ??-catenin localization, wound-healing migration, and cisplatin sensitivity testing. The A2780 background (TP53 wild-type, BRCA1/2 wild-type) makes it valuable for ovarian cancer functional genomics and high-throughput Wnt pathway screening.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    DIXDC1

    Gene Identifier

    NCBI Gene ID 85458

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 DIXDC1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of A2780 ovarian carcinoma cells in which DIXDC1 expression has been disrupted. This knockout model provides a heterogeneous pool of gene-edited cells, enabling loss-of-function studies without single-cell cloning. The polyclonal format preserves biological variability and is suitable for functional genomics, signaling analyses, and high-throughput screening in an epithelial ovarian cancer context.

The parental A2780 cell line was derived from an untreated patient with ovarian carcinoma and retains wild-type TP53 and BRCA1/2 alleles. Its cisplatin sensitivity and intact DNA damage response make it an ideal host for probing DIXDC1-regulated pathways relevant to therapeutic resistance. The adherent epithelial morphology facilitates standard imaging, proliferation, and migration assays.

DIXDC1 is a scaffold protein that enhances canonical Wnt/??-catenin signaling by binding DVL (DVL1/2/3) and AXIN (AXIN1/2), thereby inhibiting the ??-catenin destruction complex. This promotes ??-catenin stabilization and TCF/LEF-dependent transcription of targets including CCND1 and MYC. DIXDC1 also participates in non-canonical Wnt/PCP signaling via JNK and interacts with PI3K/AKT components. Upstream, WNT3A ligands activate FZD/LRP5/6 receptors to recruit DVL, positioning DIXDC1 as a key node.

In A2780 cells, DIXDC1 knockout attenuates Wnt-driven proliferation and migration, providing a platform to dissect its oncogenic roles in ovarian carcinoma. The model??s wild-type TP53 status allows independent analysis of DIXDC1 function, circumventing confounding p53 mutations. This system is particularly valuable for investigating mechanisms of cisplatin sensitivity and for evaluating Wnt pathway contributions to chemoresistance in a clinically relevant background.

Applications include TOPFlash/FOPFlash reporter assays for TCF/LEF activity, Western blotting for ??-catenin and DVL, qPCR for CCND1/MYC, immunofluorescence for ??-catenin localization, MTT proliferation and wound-healing migration assays, and cisplatin sensitivity testing. Co-immunoprecipitation can assess DIXDC1-DVL interactions. The polyclonal knockout pool is also suited for high-throughput chemical or RNAi screens to identify Wnt pathway modulators. For further details, contact Ascent Research.

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