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Cat. No. ARG40780

EHD1 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

EHD1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of the SK-HEP-1 human hepatic adenocarcinoma line, which exhibits liver sinusoidal endothelial cell characteristics. This loss-of-function model enables investigation of EHD1-dependent endocytic recycling and receptor trafficking, particularly of EGFR and integrin beta1. Disruption of EHD1 impairs recycling of surface receptors, affecting cell migration, signaling, and metabolic functions. The polyclonal knockout format is ideal for studying cancer metastasis, viral entry, and drug delivery, and is compatible with assays such as transferrin recycling, cell invasion, and flow cytometry.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SK-HEP-1

    Sex of Donor

    Male

    Age

    52 years

    Gene Name

    EHD1

    Gene Identifier

    NCBI Gene ID 10938

    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 EHD1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from SK-HEP-1 human hepatic adenocarcinoma cells. This polyclonal pool contains a heterogeneous spectrum of EHD1 gene disruptions, providing a loss-of-function model for studying endocytic recycling without clonal selection bias. The product is designed for researchers investigating receptor trafficking, membrane dynamics, and downstream signaling pathways that depend on EHD1 activity.

SK-HEP-1 is an ascites-derived cell line retaining features of liver sinusoidal endothelial cells, including roles in filtration, endocytosis, and immune cell interaction. Its endothelial-like properties and malignant origin make it a robust model for liver cancer biology, tumor microenvironment studies, and investigations of sinusoidal cell function. The expression of scavenger receptors and adhesion molecules supports research on metastatic dissemination and drug uptake mechanisms.

EHD1 encodes an ATPase that promotes vesicle fission from the endocytic recycling compartment, facilitating the return of internalized receptors to the plasma membrane. This process is regulated by membrane curvature, Arf6, Rab11, and PI3K signaling, and EHD1 directly interacts with Syndapin, Rab11-FIP2, and EHD2/EHD3/EHD4. Key downstream targets include EGFR, integrin beta1, transferrin receptor, and GLUT4. Disruption of EHD1 impairs recycling of these receptors, thereby modulating proliferative, migratory, and metabolic signaling pathways.

In SK-HEP-1 cells, loss of EHD1 allows dissection of how endocytic recycling governs liver sinusoidal endothelial functions such as receptor-mediated endocytosis, transcytosis, and immune cell engagement. The model is pertinent to cancer metastasis research, as EHD1-dependent integrin trafficking influences cell adhesion and invasion. Additionally, impaired GLUT4 recycling links to metabolic disorders, and altered EGFR trafficking affects oncogenic signaling, making this knockout population valuable for cancer biology and drug discovery.

This polyclonal knockout product is suitable for transferrin recycling and EGFR internalization assays, cell migration/invasion studies, western blotting, immunofluorescence, co-immunoprecipitation, flow cytometry, and RT-qPCR. Researchers in viral entry, drug delivery, and receptor trafficking will find it a versatile tool for mechanistic and screening studies. For further information and technical support, please contact Ascent Research.

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