Defective copper binding to apo-ceruloplasmin in a rat model and patients with Wilson's disease
Author:
Publisher
Wiley
Subject
Hepatology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1600-0676.1995.tb00660.x/fullpdf
Reference30 articles.
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2. Spontaneous hepatic copper accumulation in LEC rats with hereditary hepatitis: a model of Wilson's disease;Li;J Clin Invest,1991
3. Abnormal Copper Accumulation in the Liver of LEC Rats: A Rat Form of Wilson’s Disease
4. Single-step method of RNA isolation by acid guanidium thiocyanate-phenol-chloroform extraction;Chomczynski;Anal Biochem,1987
5. Primary structure of rat ceruloplasmin and analysis of tissue-specific gene expression during development;Fleming;J Biol Chem,1990
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1. Bis-choline tetrathiomolybdate prevents copper-induced blood–brain barrier damage;Life Science Alliance;2021-12-02
2. Molecular Architecture of the Copper-Transporting ATPase ATP7B;Clinical and Translational Perspectives on WILSON DISEASE;2019
3. Targeted inactivation of copper transporter Atp7b in hepatocytes causes liver steatosis and obesity in mice;American Journal of Physiology-Gastrointestinal and Liver Physiology;2017-07-01
4. Distinct phenotype of a Wilson disease mutation reveals a novel trafficking determinant in the copper transporter ATP7B;Proceedings of the National Academy of Sciences;2014-03-24
5. Truncating mutations in the Wilson disease gene ATP7B are associated with very low serum ceruloplasmin oxidase activity and an early onset of Wilson disease;BMC Gastroenterology;2010-01-18
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