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Cat. No. ARG40417

ECI2 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The ECI2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with disrupted ECI2 gene expression in human liver adenocarcinoma SK-HEP-1 cells. ECI2 encodes mitochondrial enoyl-CoA isomerase, a critical enzyme in unsaturated fatty acid ??-oxidation, regulated by PPAR?? and PGC-1?? and interacting with ACADs and the HADHA/HADHB trifunctional protein. Its loss impairs lipid degradation and ATP generation. This knockout model enables investigation of fatty acid oxidation disorders, metabolic reprogramming in liver cancer, and mitochondrial dysfunction. Suitable for western blotting, fatty acid oxidation assays, Seahorse metabolic flux analysis, acylcarnitine profiling, and drug screening for lipid metabolism modulators.

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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

    ECI2

    Gene Identifier

    NCBI Gene ID 10455

    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

This product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ECI2 gene in the SK-HEP-1 human liver adenocarcinoma cell line. The ECI2 knockout model is generated by CRISPR/Cas9-mediated gene disruption, resulting in a loss-of-function mutation across a heterogeneous pool of cells, enabling the study of ECI2-dependent metabolic functions without clonal selection.

SK-HEP-1 is a human liver adenocarcinoma cell line originally isolated from ascitic fluid of a patient with liver adenocarcinoma. These cells exhibit a mixed epithelial/endothelial phenotype, making them a unique model for studying both hepatocellular carcinoma and endothelial cell biology. The line is widely employed to dissect cancer metabolism, angiogenesis, and the interplay between epithelial and mesenchymal characteristics in tumor progression.

ECI2 encodes mitochondrial enoyl-CoA isomerase, which catalyzes isomerization of 3-cis- and 2-trans-enoyl-CoA esters for ??-oxidation of unsaturated fatty acids. Its expression is activated by PPAR?? and PGC-1??, while HNF4?? contributes to hepatic regulation. ECI2 collaborates with ACADs, ECHS1, and the HADHA/HADHB trifunctional protein to drive fatty acid degradation, yielding acetyl-CoA, NADH, FADH2, and ultimately ATP. This positions ECI2 as a critical node in mitochondrial energy metabolism and lipid homeostasis.

In SK-HEP-1 cells, ECI2 knockout impairs the degradation of unsaturated fatty acids, recapitulating features of fatty acid oxidation disorders and mitochondrial dysfunction. The mixed epithelial-endothelial nature of the host line makes this model particularly valuable for dissecting metabolic crosstalk between cancer cells and the tumor microenvironment. Altered lipid metabolism in these knockout cells may reveal mechanisms of lipid-induced hepatotoxicity, metabolic reprogramming in liver cancer, and the contribution of fatty acid oxidation to endothelial cell function. Consequently, this model is relevant for studying conditions such as non-alcoholic fatty liver disease, metabolic acidosis, and cancer-associated cachexia.

Researchers can employ these ECI2 knockout polyclonal cells in a variety of assays, including western blotting for protein expression verification, radiolabeled fatty acid oxidation assays (using oleate or palmitate), Seahorse metabolic flux analysis to measure oxygen consumption and ATP production, acylcarnitine profiling by LC-MS to assess fatty acid intermediates, and Oil Red O staining to visualize neutral lipid accumulation. These tools enable investigation of metabolic reprogramming, drug screening for fatty acid oxidation modulators, and functional studies of lipid handling in liver and endothelial biology. For further inquiries or to acquire this product, please contact Ascent Research.

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