The many faces of the copper metabolism protein MURR1/COMMD1
| Autor: | B van de Sluis, Cisca Wijmenga, P de Bie, L. W. J. Klomp |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2005 |
| Předmět: |
Regulator
NF-kappa B/physiology Models Genes Regulator Dog Diseases Cloning Molecular Hepatocytes/cytology Genetics (clinical) Metal Metabolism Inborn Errors Dog Diseases/genetics Metal metabolism Copper toxicity NF-kappa B Signal transducing adaptor protein Adaptor Proteins Metal Metabolism Biochemistry Models Animal Proteins/genetics Signal transduction Signal Transduction Biotechnology chemistry.chemical_element Biology Copper/metabolism Dogs Genetics medicine Animals Humans Molecular Biology Gene Adaptor Proteins Signal Transducing Animal Sodium Signal Transducing Proteins Molecular medicine.disease Copper Sodium/metabolism chemistry Genes Hepatocytes Signal Transduction/genetics Copper deficiency Carrier Proteins Regulator/physiology Inborn Errors/genetics Cloning |
| Zdroj: | Journal of Heredity. 96(7):803-11 |
| ISSN: | 0022-1503 |
| DOI: | 10.1093/jhered/esi110 |
| Popis: | Copper is an essential transition metal but is toxic in excess; therefore, its metabolism needs to be tightly regulated. Defects in the regulation of copper can lead to various disorders characterized by copper deficiency or copper excess. Recently, we characterized the COMMD1 (previously MURR1) gene as the defective gene in canine copper toxicosis. The molecular functions of COMMD1 remain unknown, but significant progress has been made in identifying the cellular processes in which COMMD1 participates, through the identification of proteins interacting with COMMD1. This review discusses how COMMD1 functions as a regulator of not only copper homeostasis but also sodium transport and the NF-kappaB signaling pathway. We outline the possible mechanisms through which COMMD1 exerts these newly identified functions. |
| Databáze: | OpenAIRE |
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