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pubmed-article:19813030pubmed:abstractTextCopper is an essential but potentially harmful trace element involved in many enzymatic processes that require redox chemistry. Cellular copper homeostasis in mammals is predominantly maintained by posttranslational regulation of copper import and export through the copper import proteins hCTR1 and hCTR2 and the copper exporters ATP7A and ATP7B. Regulation of copper uptake and export is achieved by modulation of transporter expression, copper-dependent and copper-independent trafficking of the different transporters, posttranslational modifications, and interacting proteins. In this review we systematically discuss the contribution of these different mechanisms to the regulation of copper transport.lld:pubmed
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pubmed-article:19813030pubmed:authorpubmed-author:KlompLeo W...lld:pubmed
pubmed-article:19813030pubmed:authorpubmed-author:van den...lld:pubmed
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pubmed-article:19813030pubmed:year2010lld:pubmed
pubmed-article:19813030pubmed:articleTitlePosttranslational regulation of copper transporters.lld:pubmed
pubmed-article:19813030pubmed:affiliationDepartment of Metabolic and Endocrine Diseases, University Medical Center Utrecht, The Netherlands.lld:pubmed
pubmed-article:19813030pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19813030pubmed:publicationTypeReviewlld:pubmed
pubmed-article:19813030pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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