ArticleThe Journal of biological chemistry2013
A novel transcription mechanism activated by ethanol: induction of Slc7a11 gene expression via inhibition of the DNA-binding activity of transcriptional repressor octamer-binding transcription factor 1 (OCT-1).
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
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- Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Genetic association and functional implications of TLR4 rs1927914 polymorphism on colon cancer risk.BMC cancer · 2024Article
- Apolipoprotein A-I Inhibits Transendothelial Transport of Apolipoprotein B-Carrying Lipoproteins and Enhances Its Associated High-Density Lipoprotein Formation.Journal of vascular research · 2022Article
- Current understanding of ferroptosis in the progression and treatment of pancreatic cancer.Cancer cell international · 2021Review
- Alcohol Modulation of Amyloid Precursor Protein in Alzheimer's Disease.Journal of drug and alcohol research · 2020Article
- Redistribution of Membrane Raft Microdomains by Apolipoprotein A-I In Mouse Aortic Endothelial Cells.Cardiovascular disease and medicine · 2020Article
- Molecular mechanisms of ferroptosis and its role in cancer therapy.Journal of cellular and molecular medicine · 2019Review
- Article
- Alcohol and Cocaine Exposure Modulates ABCB1 and ABCG2 Transporters in Male Alcohol-Preferring Rats.Molecular neurobiology · 2019Article
- TRAP-seq identifies cystine/glutamate antiporter as a driver of recovery from liver injury.The Journal of clinical investigation · 2018Article
- Pak1 mediates the stimulatory effect of insulin and curcumin on hepatic ChREBP expression.Journal of molecular cell biology · 2017Article
- Article
- Interleukin 1β Regulation of the System xc- Substrate-specific Subunit, xCT, in Primary Mouse Astrocytes Involves the RNA-binding Protein HuR.The Journal of biological chemistry · 2016Article
- Ethanol-Associated Changes in Glutamate Reward Neurocircuitry: A Minireview of Clinical and Preclinical Genetic Findings.Progress in molecular biology and translational science · 2016Review
- High-density lipoprotein-mediated transcellular cholesterol transport in mouse aortic endothelial cells.Biochemical and biophysical research communications · 2015Article
- Signal transducer and activator of transcription 3 and 5 regulate system Xc- and redox balance in human breast cancer cells.Molecular and cellular biochemistry · 2015Article
- A Subregion of Reelin Suppresses Lipoprotein-Induced Cholesterol Accumulation in Macrophages.PloS one · 2015Article
- Polyphenol Stilbenes: Molecular Mechanisms of Defence against Oxidative Stress and Aging-Related Diseases.Oxidative medicine and cellular longevity · 2015Review
- Up-regulation of cholesterol absorption is a mechanism for cholecystokinin-induced hypercholesterolemia.The Journal of biological chemistry · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Solute carrier family 7, member 11 (Slc7a11) is a plasma membrane cystine/glutamate exchanger that provides intracellular cystine to produce glutathione, a major cellular antioxidant. Oxidative and endoplasmic reticulum stresses up-regulate Slc7a11 expression by activation of nuclear factor erythroid 2-related factor 2 and transcription factor 4. This study examined the effect of ethanol on Slc7a11 expression and the underlying mechanism involved. Treatment of mouse hepatic stellate cells with ethanol significantly increased Slc7a11 mRNA and protein levels. Deletion of a 20-bp DNA sequence between -2044 to -2024 upstream of the transcription start site significantly increased basal activity and completely abolished the ethanol-induced activity of the Slc7a11 promoter. This deletion did not affect Slc7a11 promoter activity induced by oxidative or endoplasmic reticulum stress. DNA sequence analysis revealed a binding motif for octamer-binding transcription factor 1 (OCT-1) in the deleted fragment. Mutation of this OCT-1 binding motif resulted in a similar effect as the deletion experiment, i.e. it increased the basal promoter activity and abolished the response to ethanol. Ethanol exposure significantly inhibited OCT-1 binding to the Slc7a11 promoter region, although it did not alter OCT-1 mRNA and protein levels. OCT-1 reportedly functions as either a transcriptional enhancer or repressor, depending on the target genes. Results from this study suggest that OCT-1 functions as a repressor on the Slc7a11 promoter and that ethanol inhibits OCT-1 binding to the Slc7a11 promoter, thereby increasing Slc7a11 expression. Taken together, inhibition of the DNA binding activity of transcriptional repressor OCT-1 is a mechanism by which ethanol up-regulates Slc711 expression.
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