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Cat. No. ARG35540

KRT20 Knockout DLD-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Adenocarcinoma

The KRT20 Knockout DLD-1 Polyclonal Cells provide a CRISPR/Cas9-edited knockout population disrupting keratin 20 in the DLD-1 colorectal adenocarcinoma epithelial cell line. KRT20 is an intermediate filament protein that partners with KRT8 and integrates with desmoplakin, plakoglobin, and ??-catenin/E-cadherin adhesion complexes, functioning downstream of CDX2 and Wnt/??-catenin signaling. This polyclonal knockout model is suited for investigating epithelial differentiation, cytoskeletal integrity, EMT, and drug resistance in colorectal cancer. Key applications include immunofluorescence, migration and invasion assays, RNA-seq, and drug sensitivity profiling. For additional details, contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    DLD-1

    Age

    Adult

    Gene Name

    KRT20

    Gene Identifier

    NCBI Gene ID 54474

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 KRT20 Knockout DLD-1 Polyclonal Cells are a versatile loss-of-function model generated by CRISPR/Cas9-mediated gene disruption in the DLD-1 human colorectal adenocarcinoma epithelial cell line. This product is delivered as a polyclonal knockout cell population, enabling robust investigation of keratin 20 (KRT20) function in a tumorigenic epithelial context.

The parental DLD-1 cell line was originally derived from a male patient with Duke??s type C colorectal adenocarcinoma and is widely employed as a model system for colorectal cancer biology. DLD-1 cells retain epithelial characteristics, harbor mutations in key oncogenic and tumor suppressor pathways, and are suitable for studies of differentiation, adhesion, and drug response.

KRT20 encodes a type I intermediate filament protein that is co-expressed with its binding partner KRT8 to form obligate heteropolymers, critical for maintaining epithelial structural integrity and cell adhesion. In colorectal epithelial cells, KRT20 expression is tightly regulated by transcription factors including CDX2, GATA4, GATA6, and downstream effectors of the Wnt/??-catenin pathway such as TCF/LEF. KRT20 interacts directly with KRT8, desmoplakin, and plakoglobin, and its filament network integrates with E-cadherin/??-catenin adhesion complexes. Loss of KRT20 disrupts KRT8/KRT20 intermediate filament organization, compromising desmosomal and adherens junction stability and potentially altering Wnt/??-catenin target gene expression.

In the DLD-1 background, KRT20 knockout models the consequences of impaired epithelial differentiation often observed during colorectal cancer progression. Disruption of KRT20-mediated filament networks may promote a partial epithelial-mesenchymal transition (EMT) state, influencing cell migration, invasion, and therapeutic resistance. This polyclonal knockout population thus serves as a relevant in vitro tool to dissect the interplay between cytoskeletal architecture, cell adhesion, and oncogenic signaling in colorectal adenocarcinoma.

Researchers can apply these cells in a broad range of experimental workflows, including immunofluorescence and Western blotting for cytoskeletal protein analysis, migration and invasion assays to evaluate metastatic potential, and RNA-seq for transcriptomic profiling of differentiation and EMT programs. Additional applications include drug sensitivity screening to identify vulnerabilities associated with intermediate filament disruption and biomarker validation studies targeting KRT20-associated pathways. For technical specifications and ordering information, please contact Ascent Research.

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