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Literature summary for 7.2.2.9 extracted from

  • Cater, M.A.; La Fontaine, S.; Shield, K.; Deal, Y.; Mercer, J.F.
    ATP7B mediates vesicular sequestration of copper: insight into biliary copper excretion (2006), Gastroenterology, 130, 493-506.
    View publication on PubMed

Localization

Localization Comment Organism GeneOntology No. Textmining
pericanalicular vesicle in HepG2 cells, elevated copper levels stimulates trafficking of ATP7B to pericanalicular vesicles. Mutations of an endocytic retrieval signal in ATP7B cause the protein to constitutively localize to vesicles and not to plasma membrane. The vesicular compartment is the final trafficking destination for ATP7B Homo sapiens 33675
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Metals/Ions

Metals/Ions Comment Organism Structure
Cu in HepG2 cells, elevated copper levels stimulates trafficking of ATP7B to pericanalicular vesicles. Mechanism of biliary copper excretion involves ATP7B-mediated vesicular sequestration of copper rather than direct copper translocation across the canalicular membrane Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P35670
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Source Tissue

Source Tissue Comment Organism Textmining
Hep-G2 cell
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Homo sapiens
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Synonyms

Synonyms Comment Organism
ATP7B
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Homo sapiens