Hep G2 nuclear extract (Acetaldehyde treated)

Synonyms

Hep G2, HepG2, Acetaldehyde treated, acetaldehyde, nuclear extract, nuclear, extract, lysate, nuclear lysate, liver, liver cancer, hepatocyte, HBV, hepatitis, hepatitis B, polarization, polar, trafficking, localization, subcellular localization, liver metabolism, sigaling, signalling, signaling pathway, signalling pathway, apoptosis, cell death, cell survival, liver toxicity, liver regeneration, aldehyde, alcohol induced liver disease, alcohol, alcohol-induced, alcohol induced, alcohol-induced liver disease, ALD, autoimmune injury, gastrointestinal cancer, gastrointestinal tumor, GI, liver tumor, tumour, oxidative stress, NFkB, NF-kB, AP-1, alcohol dehydrogenase, ethanol metabolism, ROS, reactive oxygen species, SP-1, NF-1, fibrogenesis, hepatic, hepatic cancer, hepatic disease, liver disease, hypoxia, 36065

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Contents

2 x 100 µg of Hep G2 nuclear extract (Acetaldehyde treated) at 2.5 µg/µl.

Background

Hep G2 nuclear extract (Acetaldehyde treated) was prepared from cell cultures of the human hepatocellular liver carcinoma Hep G2 cell line. These cells are epithelial in morphology and can be induced to form polarized epithelium under appropriate culture conditions. Hep G2 cells are most commonly used for studies related to hepatocyte function. Because of their ability to differentiate into polarized epithelium, these cells are often used to investigate intracellular protein trafficking, specifically in relation to human liver diseases. Hep G2 is the most commonly used cell line for studying the regulation of hepatic protein synthesis, particularly the synthesis of acute phase proteins after the onset of a systemic inflammatory response. In addition, these cells are used to study liver metabolism, liver cancers, liver regeneration, liver cytotoxicity, apoptosis and as a model for hepatitis B virus (HBV) viral etiology.

Treatment of Hep G2 cells with acetaldehyde leads to various cytotoxic effects associated with alcohol-induced liver disease (ALD). Acetaldehyde, along with reactive oxygen species (ROS), is generated as a byproduct of ethanol metabolism and is a critical mediator of the induction of oxidative stress and other deleterious effects of ALD, in particular those related to autoimmune injury. The induction of oxidative stress by acetaldehyde leads to the subsequent activation of NFκB and AP-1. Activation of these transcription factors in pro-oxidant conditions leads to upregulation of inflammatory cytokines. Additionally, the formation of protein-acetaldehyde adducts triggers the activation of NF-1 and SP-1 transcription factors that is accompanied by the onset of fibrogenesis. Also, several studies have linked exposure to elevated levels of acetaldehyde, either through alcohol abuse or a defect in alcohol dehydrogenase, to an increased risk of developing liver and gastrointestinal cancers.

Application Notes

Hep G2 nuclear extract (Acetaldehyde treated) is specifically recommended for studies related to 1) ALD, 2) human liver diseases, cancers and drug therapies, 3) HBV etiology, 4) NF-κB and AP-1 signaling pathways, and 5) apoptosis.

Extract Origin

Human Liver (hepatocellular carcinoma)

Extract Composition

Hep G2 nuclear extract (Acetaldehyde treated) is supplied in Dilution Buffer (20 mM Hepes (pH 7.9), 100 mM KCl, 1 mM MgCl₂, 20% glycerol, 0.5 mM PMSF and 0.5 mM DTT). Cells were cultured in medium supplemented with 200 µM Acetaldehyde for 4 hours at 37°C immediately prior to harvesting.

Quality Control

Extracts have been quality control tested by Western blot.

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