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Zinc homeostasis and signaling in health and diseases: Zinc signaling

The essential trace element zinc (Zn) is widely required in cellular functions, and abnormal Zn homeostasis causes a variety of health problems that include growth retardation, immunodeficiency, hypogonadism, and neuronal and sensory dysfunctions. Zn homeostasis is regulated through Zn transporters,...

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Detalles Bibliográficos
Autores principales: Fukada, Toshiyuki, Yamasaki, Satoru, Nishida, Keigo, Murakami, Masaaki, Hirano, Toshio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176402/
https://www.ncbi.nlm.nih.gov/pubmed/21660546
http://dx.doi.org/10.1007/s00775-011-0797-4
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author Fukada, Toshiyuki
Yamasaki, Satoru
Nishida, Keigo
Murakami, Masaaki
Hirano, Toshio
author_facet Fukada, Toshiyuki
Yamasaki, Satoru
Nishida, Keigo
Murakami, Masaaki
Hirano, Toshio
author_sort Fukada, Toshiyuki
collection PubMed
description The essential trace element zinc (Zn) is widely required in cellular functions, and abnormal Zn homeostasis causes a variety of health problems that include growth retardation, immunodeficiency, hypogonadism, and neuronal and sensory dysfunctions. Zn homeostasis is regulated through Zn transporters, permeable channels, and metallothioneins. Recent studies highlight Zn’s dynamic activity and its role as a signaling mediator. Zn acts as an intracellular signaling molecule, capable of communicating between cells, converting extracellular stimuli to intracellular signals, and controlling intracellular events. We have proposed that intracellular Zn signaling falls into two classes, early and late Zn signaling. This review addresses recent findings regarding Zn signaling and its role in physiological processes and pathogenesis.
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spelling pubmed-31764022011-09-30 Zinc homeostasis and signaling in health and diseases: Zinc signaling Fukada, Toshiyuki Yamasaki, Satoru Nishida, Keigo Murakami, Masaaki Hirano, Toshio J Biol Inorg Chem Minireview The essential trace element zinc (Zn) is widely required in cellular functions, and abnormal Zn homeostasis causes a variety of health problems that include growth retardation, immunodeficiency, hypogonadism, and neuronal and sensory dysfunctions. Zn homeostasis is regulated through Zn transporters, permeable channels, and metallothioneins. Recent studies highlight Zn’s dynamic activity and its role as a signaling mediator. Zn acts as an intracellular signaling molecule, capable of communicating between cells, converting extracellular stimuli to intracellular signals, and controlling intracellular events. We have proposed that intracellular Zn signaling falls into two classes, early and late Zn signaling. This review addresses recent findings regarding Zn signaling and its role in physiological processes and pathogenesis. Springer-Verlag 2011-06-10 2011 /pmc/articles/PMC3176402/ /pubmed/21660546 http://dx.doi.org/10.1007/s00775-011-0797-4 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Minireview
Fukada, Toshiyuki
Yamasaki, Satoru
Nishida, Keigo
Murakami, Masaaki
Hirano, Toshio
Zinc homeostasis and signaling in health and diseases: Zinc signaling
title Zinc homeostasis and signaling in health and diseases: Zinc signaling
title_full Zinc homeostasis and signaling in health and diseases: Zinc signaling
title_fullStr Zinc homeostasis and signaling in health and diseases: Zinc signaling
title_full_unstemmed Zinc homeostasis and signaling in health and diseases: Zinc signaling
title_short Zinc homeostasis and signaling in health and diseases: Zinc signaling
title_sort zinc homeostasis and signaling in health and diseases: zinc signaling
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176402/
https://www.ncbi.nlm.nih.gov/pubmed/21660546
http://dx.doi.org/10.1007/s00775-011-0797-4
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