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Article

Copper-Induced Translocation of the Wilson Disease Protein ATP7B Independent of Murr1/COMMD1 and Rab7

31 Oct 2008

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 18974300
DOI: 10.2353/ajpath.2008.071134

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Related research

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Copper-Induced Translocation of the Wilson Disease Protein ATP7B Independent of Murr1/COMMD1 and Rab7PMID 18974300Read ↗

Clusterin and COMMD1 independently regulate degradation of the mammalian copper ATPases ATP7A and ATP7B.Semantic proximity Read ↗

A glimpse into the regulation of the Wilson disease protein, ATP7B, sheds light on the complexity of mammalian apical trafficking pathways.Semantic proximity Read ↗

Dysfunction of ATP7B Splicing Variant Caused by Enhanced Interaction With COMMD1 in Wilson DiseaseSemantic proximity Read ↗

Molecular pathogenesis of Wilson and Menkes disease: correlation of mutations with molecular defects and disease phenotypes.Semantic proximity Read ↗

ATP7A-related copper transport diseases—emerging concepts and future trendsSemantic proximity Read ↗

Polarized trafficking and copper transport activity of ATP7B: A mutational approach to establish genotype-phenotype correlation in Wilson disease.Semantic proximity Read ↗

Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis.Semantic proximity Read ↗

Distinct Wilson's disease mutations in ATP7B are associated with enhanced binding to COMMD1 and reduced stability of ATP7B.Semantic proximity Read ↗

Trafficking of the copper-ATPases, ATP7A and ATP7B: role in copper homeostasis.Semantic proximity Read ↗

A systems biology approach reveals new endoplasmic reticulum-associated targets for the correction of the ATP7B mutant causing Wilson disease.Semantic proximity Read ↗

Role and mechanisms of cuproptosis in the pathogenesis of Wilson's disease (Review)Semantic proximity Read ↗

Molecular mechanisms of copper homeostasis.Semantic proximity Read ↗

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