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Cat. No. ARG38777

DIP2A Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DIP2A Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma HT29 line, featuring disruption of the DIP2A gene. DIP2A interacts with DAB2 and functions in Frizzled receptor signaling, modulating Wnt/planar cell polarity and Hippo pathways, and its loss alters Rho GTPases and YAP/TAZ activity. These polyclonal knockout cells provide a physiologically relevant model for investigating DIP2A??s role in colorectal cancer cell polarity, endocytosis, and differentiation. They are suited for assays such as Western blotting, immunofluorescence, migration, and proliferation studies, enabling dissection of oncogenic signaling and potential drug sensitivities.

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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

    DIP2A

    Gene Identifier

    NCBI Gene ID 23181

    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 DIP2A Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma line, featuring targeted disruption of the DIP2A gene. As a polyclonal pool, these cells provide a heterogeneous loss-of-function model suitable for population-level phenotypic analyses of DIP2A-dependent processes in intestinal epithelial biology and colorectal cancer.

The host HT29 cell line originates from a primary colorectal adenocarcinoma of a 44-year-old female and is a well-established model for intestinal epithelial cell biology. HT29 cells exhibit absorptive and secretory functions and can form polarized monolayers, making them valuable for studies of barrier integrity, cell adhesion, and transport. Their cancerous origin underpins their widespread use in colorectal cancer research, including tumorigenesis, metastasis, and drug response studies.

DIP2A encodes a protein that interacts with Disabled-2 (DAB2) and functions in Frizzled receptor signaling, modulating Wnt/planar cell polarity (PCP) and Hippo pathways. It is regulated by WNT ligands such as WNT3A and microRNA MIR-433. DIP2A forms complexes with DAB2, Frizzled receptors, and clathrin adaptor AP2, and its disruption influences the activity of Rho GTPases RAC1 and RHOA and Hippo effectors YAP and TAZ. As a result, DIP2A loss can perturb cell polarity, endocytic trafficking, and transcriptional programs governing proliferation.

In HT29 colorectal cancer cells, DIP2A knockout provides a model to dissect how disruption of Wnt/PCP and Hippo signaling affects malignant phenotypes. The polarized epithelial character of HT29 cells makes them ideal for examining DIP2A??s role in cell polarity and directional migration, key processes in invasion and metastasis. Additionally, DIP2A??s interaction with clathrin and AP2 suggests a role in receptor trafficking, potentially modulating oncogenic Wnt signaling. These polyclonal cells are thus valuable for research into colorectal and gastric cancers.

Researchers can utilize these polyclonal knockout cells in Western blotting to assess DIP2A depletion and changes in DAB2, RAC1, and phospho-YAP. RT-qPCR enables profiling of Wnt/PCP target genes. Immunofluorescence staining for polarity markers (e.g., ZO-1) can reveal planar polarity alterations. Migration, invasion, and proliferation assays are directly applicable for studying metastatic behavior. Co-immunoprecipitation can map protein complexes involving DAB2 and Frizzled receptors. For further details, contact Ascent Research.

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