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Cat. No. ARG38917

DLGAP4 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The DLGAP4 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population disrupting DLGAP4 in the HT29 colorectal adenocarcinoma cell line. DLGAP4 encodes a scaffold protein that links surface receptors to the actin cytoskeleton via PSD-95 (DLG4) and SHANK, and modulates Wnt/??-catenin signaling. This polyclonal model in HT29 cells, a well-established colorectal cancer line, is designed for studies of cell adhesion, migration, Wnt pathway activity, and drug sensitivity. Typical applications include TOP/FOP reporter assays, scratch wound healing, and chemosensitivity testing against 5-FU and oxaliplatin.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    DLGAP4

    Gene Identifier

    NCBI Gene ID 22839

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 DLGAP4 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human DLGAP4 gene in HT29 colorectal adenocarcinoma cells. This heterogeneous pool provides a robust loss-of-function model for assessing DLGAP4 function without clonal selection bias. Supplied as a polyclonal population, it enables evaluation of collective DLGAP4 ablation effects on cellular phenotypes.

HT29 is an adherent epithelial colorectal adenocarcinoma cell line derived from the primary tumor of a 44-year-old female. It is a widely used model for colorectal cancer biology, epithelial barrier function, and differentiation studies. The cell line exhibits canonical Wnt pathway dysregulation, making it relevant for investigating Wnt/??-catenin signaling components. Its adherent growth properties also support assays for cell adhesion, migration, and drug response.

DLGAP4 encodes SAPAP4, a postsynaptic scaffold protein that organizes synaptic signaling and the cytoskeleton through interactions with DLG4 (PSD-95) and SHANK proteins. Beyond neurons, it regulates the actin cytoskeleton and Wnt/??-catenin signaling. DLGAP4 forms complexes with SHANK1/2/3, DLGAP1, HOMER1, and CTNNB1, linking cell surface receptors to intracellular networks. It is regulated by NMDA receptor signaling, Wnt ligands, and CaM kinases, and its downstream effects include actin remodeling, SHANK-mediated signaling, and transcription of Wnt targets MYC and CCND1. In HT29 cells, DLGAP4 disruption may impair Wnt activity and weaken cell adhesion, contributing to cancer phenotypes.

Combining DLGAP4 scaffolding roles with the aberrant Wnt signaling of HT29 cells creates a platform to dissect colorectal cancer mechanisms. DLGAP4 loss is expected to alter adhesion, migration, and proliferation, facilitating tumorigenesis studies. This model uniquely bridges synaptic scaffold biology and epithelial cancer, allowing exploration of adherens junction?CWnt crosstalk in a relevant genetic context.

Applications include functional characterization of DLGAP4, colorectal cancer cell biology, and translational research. Assays such as immunofluorescence, RNA-seq, western blotting, scratch wound healing, and cell adhesion assays evaluate the impact of DLGAP4 loss. Wnt pathway studies employ TOP/FOP reporter assays, while MTT and flow cytometry assess proliferation and apoptosis. Drug sensitivity screening against 5-fluorouracil and oxaliplatin is also supported. For further information, contact Ascent Research.

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