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Cat. No. ARG27751

ABHD4 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

This product consists of a polyclonal population of Huh-7 hepatocellular carcinoma cells with CRISPR/Cas9-mediated disruption of the ABHD4 gene. ABHD4 is a lipase that hydrolyzes N?acyl?phosphatidylethanolamine (NAPE) to generate N?acylethanolamines such as anandamide, linking it to endocannabinoid signaling and glycerophospholipid metabolism. The knockout model enables investigation of ABHD4??s role in liver cancer biology, lipid metabolism, and endocannabinoid signaling pathways. Applications include N?acylethanolamine quantification by LC?MS, lipase activity assays, and drug?induced hepatotoxicity screening, making it a versatile tool for hepatic and metabolic research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    ABHD4

    Gene Identifier

    NCBI Gene ID 63874

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 ABHD4 Knockout Huh-7 Polyclonal Cells are a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the human ABHD4 gene in the Huh-7 hepatocellular carcinoma cell line. This polyclonal pool offers a heterogeneous loss-of-function model suitable for studying ABHD4-dependent processes without clonal selection biases. The edited population can be used directly in functional assays or subjected to downstream enrichment strategies.

Huh-7 is a well-differentiated hepatocyte-derived cellular carcinoma cell line originally isolated from a liver tumor in a 57-year-old Japanese male. It is widely employed as a model for hepatocellular carcinoma (HCC), liver metabolism, and drug metabolism studies. Huh-7 cells retain many characteristics of primary hepatocytes, including expression of key metabolic enzymes and the ability to synthesize and secrete plasma proteins, making them a valuable system for investigating hepatic lipid handling and hepatotoxicity screening.

ABHD4 encodes an ??/??-hydrolase domain-containing lipase that hydrolyzes N-acyl-phosphatidylethanolamine (NAPE) to produce N-acylethanolamines (NAEs), including the endocannabinoid anandamide. This reaction is central to the N-acylethanolamine biosynthesis pathway and intersects with glycerophospholipid metabolism. ABHD4 functions downstream of NAPE-PLD and upstream of fatty acid amide hydrolase (FAAH) and other phospholipases. Anandamide generated by ABHD4 activates cannabinoid receptors, thereby modulating endocannabinoid signaling and lipid metabolism. The enzyme also exhibits activity toward lyso-phosphatidylserine, further implicating it in lysophospholipid metabolism. Potential upstream regulators include peroxisome proliferator-activated receptors (PPARs), linking ABHD4 to broader metabolic transcriptional networks.

In the context of Huh-7 hepatocellular carcinoma cells, ABHD4 disruption provides insights into the interplay between lipid metabolism and liver cancer biology. Given the liver??s central role in lipid processing and the dysregulation of endocannabinoid signaling in hepatic diseases, this knockout model enables detailed exploration of how NAE production influences hepatocellular carcinoma cell growth, survival, and metabolic reprogramming. Because Huh-7 cells are widely used in toxicology, ABHD4 knockout cells also serve as a platform to investigate the enzyme??s contribution to drug-induced lipid disturbances and hepatotoxicity.

Researchers can employ these polyclonal ABHD4 knockout Huh-7 cells in a range of experimental workflows, including LC?MS?based quantification of N?acylethanolamines, lipase activity measurements, western blotting, RT?qPCR, and global lipidomics. The cells are suitable for endocannabinoid system research, lipid metabolism studies, and liver cancer cell biology, as well as for screening pharmacological agents that target NAE?related pathways. The heterogeneous population can be challenged with lipid substrates, receptor agonists, or chemotherapeutic agents to assess functional outcomes in parallel with wild?type controls. For further details or technical support, please contact Ascent Research.

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