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Article

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

Experimental cell research - 15 Jan 2009

Yanagimoto Chikatoshi, Harada Masaru, Kumemura Hiroto, Koga Hironori, Kawaguchi Takumi, Terada Kunihiko, Hanada Shinichiro, Taniguchi Eitaro, Koizumi Yukio, Koyota Souichi, Ninomiya Haruaki, Ueno Takato, Sugiyama Toshihiro, Sata Michio

Abstract excerpt

Wilson disease is a genetic disorder characterized by the accumulation of copper in the body by defective biliary copper excretion. Wilson disease gene product (ATP7B) functions in copper incorporation to ceruloplasmin (Cp) and biliary copper excretion. However, copper metabolism in hepatocytes h...

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Source

Identifiers

PMID: 19007772
DOI: 10.1016/j.yexcr.2008.10.022

Genes

NPC1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19007772-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Niemann-Pick C1 protein transports copper to the secretory compartment from late endosomes where ATP7B resides.PMID 19007772Read ↗

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

Wilson disease protein ATP7B utilizes lysosomal exocytosis to maintain copper homeostasis.Semantic 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 is localized in the late endosomes in a polarized human hepatocyte cell line.Semantic proximity Read ↗

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

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

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

Defective cellular localization of mutant ATP7B in Wilson's disease patients and hepatoma cell lines.Semantic proximity Read ↗

Retinoids rescue ceruloplasmin secretion and alleviate oxidative stress in Wilson’s disease-specific hepatocytesSemantic 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 ↗

Wilson disease-causing mutations in the carboxyl terminus of ATP7B regulates its localization and Golgi exit selectively in the unpolarized cells.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 ↗

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