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Int. J. Mol. Sci. 2017, 18(12), 2708;

Recent Advances in the Role of SLC39A/ZIP Zinc Transporters In Vivo

Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima 770-8514, Japan
Division of Pathology, Department of Oral Diagnostic Sciences, School of Dentistry, Showa University, Tokyo 142-8555, Japan
RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa 230-0042, Japan
Author to whom correspondence should be addressed.
Received: 8 November 2017 / Revised: 27 November 2017 / Accepted: 8 December 2017 / Published: 13 December 2017
(This article belongs to the Special Issue Zinc Signaling in Physiology and Pathogenesis)
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Zinc (Zn), which is an essential trace element, is involved in numerous mammalian physiological events; therefore, either a deficiency or excess of Zn impairs cellular machineries and influences physiological events, such as systemic growth, bone homeostasis, skin formation, immune responses, endocrine function, and neuronal function. Zn transporters are thought to mainly contribute to Zn homeostasis within cells and in the whole body. Recent genetic, cellular, and molecular studies of Zn transporters highlight the dynamic role of Zn as a signaling mediator linking several cellular events and signaling pathways. Dysfunction in Zn transporters causes various diseases. This review aims to provide an update of Zn transporters and Zn signaling studies and discusses the remaining questions and future directions by focusing on recent progress in determining the roles of SLC39A/ZIP family members in vivo. View Full-Text
Keywords: zinc transporter; SLC39A/ZIP; zinc signaling; physiology; diseases zinc transporter; SLC39A/ZIP; zinc signaling; physiology; diseases

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Takagishi, T.; Hara, T.; Fukada, T. Recent Advances in the Role of SLC39A/ZIP Zinc Transporters In Vivo. Int. J. Mol. Sci. 2017, 18, 2708.

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