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Article

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

International journal of molecular medicine - 1 Mar 2003

Harada Masaru, Kumemura Hiroto, Sakisaka Shotaro, Shishido Shoichiro, Taniguchi Eitaro, Kawaguchi Takumi, Hanada Shinichiro, Koga Hironori, Kumashiro Ryukichi, Ueno Takato, Suganuma Tatsuo, Furuta Koh, Namba Masayoshi, 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. The gene responsible for Wilson disease has been cloned, however, the precise localization of this gene product ATP7B, a copper-transporting ATPase, is still controversial. We examined the localization of ATP7B by expressing a chimeric protein, ATP7B-tagged with green...

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PMID: 12579329

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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Related research

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Wilson disease protein ATP7B is localized in the late endosomes in a polarized human hepatocyte cell line.PMID 12579329Read ↗

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

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

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

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

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 ↗

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

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

Intracellular distribution of the Wilson’s disease gene product (atpase7b) after in vitro and in vivo exogenous expression in hepatocytes from the LEC rat, an animal model of Wilson’s diseaseSemantic 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 ↗

Role of ATP7B in biliary copper excretion in a human hepatoma cell line and normal rat hepatocytesSemantic proximity Read ↗

EGFP tags affect cellular localization of ATP7B mutants.Semantic proximity Read ↗

Rescue of ATP7B function in hepatocyte-like cells from Wilson's disease induced pluripotent stem cells using gene therapy or the chaperone drug curcumin.Semantic proximity Read ↗

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