Elevated copper impairs hepatic nuclear receptor function in Wilson's disease.
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Summary
It is demonstrated that copper-mediated nuclear receptor dysfunction disrupts liver function in Wilson's disease and potentially in other disorders associated with increased hepatic copper levels.
- Type
- article
- Published
- 2015-09-01
- Cited by
- 70
- References
- 61
- Access
- Open access
- OpenAlex
- https://openalex.org/W26241054
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:3705504
Keywords
Business, Process management, Industrial organization
References
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- ZINC THERAPY INDUCTION OF INTESTINAL METALLOTHIONEIN IN WILSON'S DISEASE
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- The nature of the copper complexes in bile and their relationship to the absorption and excretion of copper in normal subjects and in Wilson's disease
- Bile acid transport in sister of P-glycoprotein (ABCB11) knockout mice.
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Cited by
- Colony‐stimulating factor 1 should be considered when studying the miR‐28‐5p‐IL‐34‐macrophage feedback loop in hepatocellular carcinoma
- Broadening the implications of gene discovery
- Liver X receptors and copper metabolism: New frontiers for the oxysterol receptors
- The Activity of Menkes Disease Protein ATP7A Is Essential for Redox Balance in Mitochondria*
- The Role of Copper Chaperone Atox1 in Coupling Redox Homeostasis to Intracellular Copper Distribution
- Wilson Disease: Epigenetic effects of choline supplementation on phenotype and clinical course in a mouse model
- Lipid and copper metabolism in humans with wilson disease: Enigmatic relationship
- Genetic profiling of children with advanced cholestatic liver disease
- Animal models of Wilson disease.
- Targeted inactivation of copper transporter Atp7b in hepatocytes causes liver steatosis and obesity in mice.
- Cellular copper homeostasis: current concepts on its interplay with glutathione homeostasis and its implication in physiology and human diseases.
- Troxerutin with copper generates oxidative stress in cancer cells: Its possible chemotherapeutic mechanism against hepatocellular carcinoma
- The Extracellular Domain of Human High Affinity Copper Transporter (hNdCTR1), Synthesized by E. coli Cells, Chelates Silver and Copper Ions In Vivo
- Neurotoxicity of Copper.
- Animal models of Wilson disease
- Copper concentrations in Egyptian infants with cholestasis: A single center study.
- Evaluation of the accuracy of exchangeable copper and relative exchangeable copper (REC) in a mouse model of Wilson's disease.
- Altered zinc balance in the Atp7b−/− mouse model reveals a mechanism of copper toxicity in Wilson Disease
- Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD
- Update on the Diagnosis and Management of Wilson Disease
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