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Article

The Wilson disease protein ATP7B resides in the late endosomes with Rab7 and the Niemann-Pick C1 protein.

The American journal of pathology - 1 Feb 2005

Harada Masaru, Kawaguchi Takumi, Kumemura Hiroto, Terada Kunihiko, Ninomiya Haruaki, Taniguchi Eitaro, Hanada Shinichiro, Baba Shinji, Maeyama Michiko, Koga Hironori, Ueno Takato, Furuta Koh, Suganuma Tatsuo, Sugiyama Toshihiro, Sata Michio

Abstract excerpt

Wilson disease is a genetic disorder characterized by the accumulation of copper in the body due to a defect of biliary copper excretion. Although the Wilson disease gene has been cloned, the cellular localization of the gene product (ATP7B) has not been fully clarified. Therefore, the precise physiological action of ATP7B is still unknown. We examined the distribution of ATP7B using an anti-ATP7B antibody, green...

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Identifiers

PMID: 15681833
DOI: 10.1016/S0002-9440(10)62272-9
PMCID: PMC1602322

Genes

NPC1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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The Wilson disease protein ATP7B resides in the late endosomes with Rab7 and the Niemann-Pick C1 protein.PMID 15681833Read ↗

Niemann-Pick C1 protein transports copper to the secretory compartment from late endosomes where ATP7B resides.Semantic proximity Read ↗

Wilson disease protein ATP7B is localized in the late endosomes in a polarized human hepatocyte cell line.Semantic proximity Read ↗

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

A mutation of the Wilson disease protein, ATP7B, is degraded in the proteasomes and forms protein aggregates.Semantic proximity Read ↗

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

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Critical roles for the COOH terminus of the Cu-ATPase ATP7B in protein stability, trans-Golgi network retention, copper sensing, and retrograde trafficking.Semantic proximity Read ↗

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