11: Metallothionein-3, Zinc, and Copper in the Central Nervous System
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Published:19 Jan 2009
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M. Vašák and G. Meloni, in Metallothioneins and Related Chelators, ed. A. Sigel, H. Sigel, R. K. O. Sigel, A. Sigel, H. Sigel, R. K. O. Sigel, ... R. K. O. Sigel, The Royal Society of Chemistry, 2009, vol. 5, pp. 319-351.
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Metallothionein-3 (MT-3), also known as the neuronal growth inhibitory factor, has been discovered by Uchida and coworkers in 1991 in their search for a cellular component responsible for antagonizing aberrant neuritic sprouting and increased survival of cultured neurons stimulated by Alzheimer's disease (AD) brain extract. Since this initial discovery further studies showed that MT-3 possesses peculiar structural and functional properties not shared by other members of the mammalian MT family. Several lines of evidence suggest that the metal-binding protein MT-3 plays a vital role in zinc and copper homeostasis in the brain. Although far from being understood, the unusual structural properties of MT-3 are responsible for its neuronal growth inhibitory activity, involvement in trafficking of zinc vesicles in the central nervous system, protection against copper-mediated toxicity in AD and in controlling abnormal metal-protein interactions in other neurodegenerative disorders.
Metallothionein-3 (MT-3), also known as the neuronal growth inhibitory factor, has been discovered by Uchida and coworkers in 1991 in their search for a cellular component responsible for antagonizing aberrant neuritic sprouting and increased survival of cultured neurons stimulated by Alzheimer's disease (AD) brain extract. Since this initial discovery further studies showed that MT-3 possesses peculiar structural and functional properties not shared by other members of the mammalian MT family. Several lines of evidence suggest that the metal-binding protein MT-3 plays a vital role in zinc and copper homeostasis in the brain. Although far from being understood, the unusual structural properties of MT-3 are responsible for its neuronal growth inhibitory activity, involvement in trafficking of zinc vesicles in the central nervous system, protection against copper-mediated toxicity in AD and in controlling abnormal metal-protein interactions in other neurodegenerative disorders.
Metallothionein-3 (MT-3), also known as the neuronal growth inhibitory factor, has been discovered by Uchida and coworkers in 1991 in their search for a cellular component responsible for antagonizing aberrant neuritic sprouting and increased survival of cultured neurons stimulated by Alzheimer's disease (AD) brain extract. Since this initial discovery further studies showed that MT-3 possesses peculiar structural and functional properties not shared by other members of the mammalian MT family. Several lines of evidence suggest that the metal-binding protein MT-3 plays a vital role in zinc and copper homeostasis in the brain. Although far from being understood, the unusual structural properties of MT-3 are responsible for its neuronal growth inhibitory activity, involvement in trafficking of zinc vesicles in the central nervous system, protection against copper-mediated toxicity in AD and in controlling abnormal metal-protein interactions in other neurodegenerative disorders.
Metallothionein-3 (MT-3), also known as the neuronal growth inhibitory factor, has been discovered by Uchida and coworkers in 1991 in their search for a cellular component responsible for antagonizing aberrant neuritic sprouting and increased survival of cultured neurons stimulated by Alzheimer's disease (AD) brain extract. Since this initial discovery further studies showed that MT-3 possesses peculiar structural and functional properties not shared by other members of the mammalian MT family. Several lines of evidence suggest that the metal-binding protein MT-3 plays a vital role in zinc and copper homeostasis in the brain. Although far from being understood, the unusual structural properties of MT-3 are responsible for its neuronal growth inhibitory activity, involvement in trafficking of zinc vesicles in the central nervous system, protection against copper-mediated toxicity in AD and in controlling abnormal metal-protein interactions in other neurodegenerative disorders.