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Article

A conditional mutation affecting localization of the Menkes disease copper ATPase. Suppression by copper supplementation.

The Journal of biological chemistry - 15 Nov 2002

Kim Byung-Eun, Smith Kathryn, Meagher Carisa K, Petris Michael J

Abstract excerpt

Copper is an essential co-factor for several key metabolic processes. This requirement in humans is underscored by Menkes disease, an X-linked copper deficiency disorder caused by mutations in the copper transporting P-type ATPase, MNK. MNK is located in the trans-Golgi network where it transports copper to secreted cuproenzymes. Increases in copper concentration stimulate the trafficking of MNK to the plasma...

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Identifiers

PMID: 12221109
DOI: 10.1074/jbc.M208737200

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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A conditional mutation affecting localization of the Menkes disease copper ATPase. Suppression by copper supplementation.PMID 12221109Read ↗

A C-terminal di-leucine is required for localization of the Menkes protein in the trans-Golgi network.Semantic proximity Read ↗

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Characterization of ATP7A missense mutants suggests a correlation between intracellular trafficking and severity of Menkes disease.Semantic proximity Read ↗

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The copper-transporting capacity of ATP7A mutants associated with Menkes disease is ameliorated by COMMD1 as a result of improved protein expression.Semantic proximity Read ↗

Trafficking of the copper-ATPases, ATP7A and ATP7B: role in copper homeostasis.Semantic proximity Read ↗

The regulation of catalytic activity of the menkes copper-translocating P-type ATPase. Role of high affinity copper-binding sites.Semantic proximity Read ↗

Functional expression of the Wilson disease protein reveals mislocalization and impaired copper-dependent trafficking of the common H1069Q mutation.Semantic proximity Read ↗

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