Copper-induced apical trafficking of ATP7B in polarized hepatoma cells provides a mechanism for biliary copper excretion
Copper-induced apical trafficking of ATP7B in polarized hepatoma cells provides a mechanism for biliary copper excretion
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DOI：
10.1053/gast.2000.17834
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发表时间：
2000-09-01
期刊：
影响因子：
29.4
通讯作者：
Vonk, RJ
中科院分区：
文献类型：
--
作者：
Roelofsen, H;Wolters, H;Vonk, RJ
Background & Aims: Mutations in the ATP7B gene, encoding a copper-transporting P-type adenosine triphosphatase, lead to excessive hepatic copper accumulation because of impaired biliary copper excretion in Wilson's disease. In human liver, ATP7B is predominantly localized to the trans-Golgi network, which appears incompatible with a role of ATP7B in biliary copper excretion. The aim of this study was to elucidate this discrepancy. Methods: Immunofluorescence and electron-microscopic methods were used to study the effects of excess copper on ATP7B localization in polarized HepG2 hepatoma cells. Results: ATP7B is localized to the trans-Golgi network only when extracellular copper concentration is low (
