Quick Order Cart

Cat. No. ARG32573

HK1 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

CRISPR/Cas9-edited HK1 knockout polyclonal cell population in SK-HEP-1 liver adenocarcinoma cells. The polyclonal knockout pool enables robust loss-of-function analysis. HK1 phosphorylates glucose to glucose-6-phosphate as the rate-limiting glycolytic step, regulated by insulin, hypoxia, and PI3K/Akt. It interacts with VDAC and BAD, linking metabolism to apoptosis, and sustains the Warburg effect. This model facilitates studies of glycolytic inhibition, metabolic reprogramming, and cancer metabolism therapies. Suitable for hexokinase activity, glucose uptake, lactate production, and Seahorse assays. Ideal for investigating hexokinase deficiency, diabetes, and liver cancer metabolic dependencies.

Inquire Now

In stock

Ships next business day


Ask a Question

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

    HK1

    Gene Identifier

    NCBI Gene ID 3098

    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 HK1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatocellular carcinoma line, with targeted disruption of the HK1 gene. This product provides a loss-of-function model for studying hexokinase 1 (HK1) in cellular metabolism and cancer biology. The heterogeneous polyclonal pool, generated via CRISPR/Cas9-mediated gene disruption, avoids clonal selection biases and is ideal for robust functional investigations.

SK-HEP-1 is a human hepatic adenocarcinoma cell line originally established from the ascites of a patient with liver cancer. This epithelial cell line retains key oncogenic features, including deregulated growth signaling and aberrant metabolism, making it a widely employed model for hepatocellular carcinoma research. Its malignant origin provides a pathophysiologically relevant platform for interrogating the metabolic dependencies altered by HK1 loss.

HK1 phosphorylates glucose to glucose-6-phosphate (G6P), catalyzing the rate-limiting step of glycolysis and committing glucose to catabolism. HK1 is regulated by insulin/PI3K/Akt signaling, which promotes mitochondrial binding, and by hypoxia via HIF1?? transcriptional induction. At the outer mitochondrial membrane, HK1 interacts with VDAC, BAD, and porin, linking metabolism to apoptosis. Downstream, G6P feeds glycolysis (via PFK and pyruvate kinase) and the pentose phosphate pathway (via G6PD), influencing redox balance and biosynthesis. Thus, HK1 integrates hormonal, hypoxic, and nutrient signals to control energy production.

In SK-HEP-1 cells, HK1 upregulation contributes to the Warburg effect, sustaining aerobic glycolysis for rapid proliferation. Disruption of HK1 in this polyclonal model impairs glycolytic flux and lactate production, likely shifting cells toward oxidative phosphorylation and increasing sensitivity to metabolic stress. This makes the model valuable for exploring cancer metabolic dependencies, hexokinase deficiency, and diabetes-related metabolic dysfunction, particularly in a hepatic context.

These knockout cells are suitable for a variety of downstream applications, including investigation of glycolytic inhibition, metabolic reprogramming, and assessment of anti-cancer metabolic therapies. Representative assays such as western blotting for HK1 expression, hexokinase activity assays, glucose uptake and lactate production measurements, Seahorse metabolic flux analysis, RT-qPCR, and immunofluorescence can be readily applied. The polyclonal cell population offers experimental consistency and is amenable to high-throughput screening. For detailed technical specifications and support, please contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)