ArticleWorld journal of gastroenterology2016
Functional analysis and drug response to zinc and D-penicillamine in stable ATP7B mutant hepatic cell lines.
Article in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- The Genomic Landscape of Wilson Disease in a Pan India Disease Cohort and Population-Scale Data.Movement disorders clinical practice · 2025Article
- Wilson's Disease-Genetic Puzzles with Diagnostic Implications.Diagnostics (Basel, Switzerland) · 2023Review
- Crossroads between membrane trafficking machinery and copper homeostasis in the nerve system.Open biology · 2021Review
- Pharmacoproteomics pinpoints HSP70 interaction for correction of the most frequent Wilson disease-causing mutant of ATP7B.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Disulfiram causes selective hypoxic cancer cell toxicity and radio-chemo-sensitization via redox cycling of copper.Free radical biology & medicine · 2020Article
- Article
- Trafficking mechanisms of P-type ATPase copper transporters.Current opinion in cell biology · 2019Review
- An αB-Crystallin Peptide Rescues Compartmentalization and Trafficking Response to Cu Overload of ATP7B-H1069Q, the Most Frequent Cause of Wilson Disease in the Caucasian Population.International journal of molecular sciences · 2018Article
- Characterization of the most frequent ATP7B mutation causing Wilson disease in hepatocytes from patient induced pluripotent stem cells.Scientific reports · 2018Article
- Copper(I)-binding properties of de-coppering drugs for the treatment of Wilson disease. α-Lipoic acid as a potential anti-copper agent.Scientific reports · 2018Article
- Functional Characterization of NovelFrontiers in pediatrics · 2018Article
- Advances in Treatment of Wilson Disease.Tremor and other hyperkinetic movements (New York, N.Y.) · 2018Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the effect of anti-copper treatment for survival of hepatic cells expressing different ATP7B mutations in cell culture.
methodsThe most common Wilson disease (WD) mutations p.H1069Q, p.R778L and p.C271*, found in the ATP7B gene encoding a liver copper transporter, were studied. The mutations represent major genotypes of the United States and Europe, China, and India, respectively. A human hepatoma cell line previously established to carry a knockout of ATP7B was used to stably express WD mutants. mRNA and protein expression of mutant ATP7B, survival of cells, apoptosis, and protein trafficking were determined.
resultsLow temperature increased ATP7B protein expression in several mutants. Intracellular ATP7B localization was significantly impaired in the mutants. Mutants were classified as high, moderate, and no survival based on their viability on exposure to toxic copper. Survival of mutant p.H1069Q and to a lesser extent p.C271* improved by D-penicillamine (DPA) treatment, while mutant p.R778L showed a pronounced response to zinc (Zn) treatment. Overall, DPA treatment resulted in higher cell survival as compared to Zn treatment; however, only combined Zn + DPA treatment fully restored cell viability.
conclusionThe data indicate that the basic impact of a genotype might be characterized by analysis of mutant hepatic cell lines.
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