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Cat. No. ARG35191

KRT20 Knockout 786-O Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

  • Disease:

    Renal cell carcinoma

The KRT20 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in the 786-O human clear cell renal cell carcinoma line, providing a loss-of-function model for keratin 20 (KRT20) studies. This model leverages the VHL-deficient epithelial background to explore KRT20??s role in intermediate filament organization and epithelial differentiation. KRT20 heterodimerizes with KRT8 and is regulated by CDX2 and Notch signaling, interacting with desmoplakin and plakoglobin to maintain cytoskeletal integrity. Applications include Western blot, migration assays, and drug screening to investigate epithelial barrier function and cancer biomarker pathways.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    786-O

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    In situ; Kidney

    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 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human cell line, engineered to disrupt the KRT20 gene. This heterogeneous pool provides a loss-of-function model for studying keratin 20 biology without clonal selection bias, suitable for assays requiring population-level analysis of gene disruption.

The 786-O parental line is a clear cell renal cell carcinoma epithelial cell line established from a primary kidney adenocarcinoma of a 58-year-old male. These cells are VHL-deficient, leading to constitutive HIF pathway activation, and serve as a widely used model for renal cell carcinoma research, characterized by dysregulated angiogenesis and metabolic alterations.

KRT20 encodes keratin 20, a type I intermediate filament protein that obligately heterodimerizes with keratin 8 (KRT8) to assemble into the epithelial intermediate filament network. Its expression is transcriptionally activated by CDX2 and modulated by Notch signaling, retinoic acid, and GATA factors. KRT20 interacts with desmosomal proteins desmoplakin and plakoglobin, and associates with cytoskeletal adaptors to maintain epithelial barrier function and structural integrity. The KRT20/KRT8 heterodimers integrate into desmosomes and hemidesmosomes, anchoring the cytoskeleton to intercellular junctions and extracellular matrix, thus participating in intermediate filament organization and epithelial differentiation.

In the VHL-deficient 786-O renal carcinoma context, KRT20 knockout allows dissection of epithelial differentiation programs against a background of HIF-driven oncogenic signaling. Despite low endogenous KRT20, disruption enables assessment of residual or inducible keratin 20 functions in cytoskeletal dynamics, migration, and epithelial-mesenchymal transition. This model helps elucidate mechanisms by which intermediate filament networks influence tumor cell behavior and may reveal vulnerabilities in VHL-deficient epithelial cancers.

Researchers can employ these polyclonal knockout cells for Western blot, immunofluorescence, and RT-qPCR confirmation of KRT20 depletion, co-immunoprecipitation with KRT8 to examine filament assembly, and functional assays such as migration and invasion studies. Applications include cancer biomarker identification, epithelial differentiation research, and drug screening in renal cell carcinoma. For detailed technical inquiries or custom cell line requests, please contact Ascent Research.

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