Zinc homeostasis and signaling in health and diseases

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

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.

Related collections

Most cited references 130

Record: found
Abstract: found
Article: not found

A genome-wide association study identifies novel risk loci for type 2 diabetes.

Robert Sladek, Ghislain Rocheleau, Johan Rung … (2007)

Type 2 diabetes mellitus results from the interaction of environmental factors with a combination of genetic variants, most of which were hitherto unknown. A systematic search for these variants was recently made possible by the development of high-density arrays that permit the genotyping of hundreds of thousands of polymorphisms. We tested 392,935 single-nucleotide polymorphisms in a French case-control cohort. Markers with the most significant difference in genotype frequencies between cases of type 2 diabetes and controls were fast-tracked for testing in a second cohort. This identified four loci containing variants that confer type 2 diabetes risk, in addition to confirming the known association with the TCF7L2 gene. These loci include a non-synonymous polymorphism in the zinc transporter SLC30A8, which is expressed exclusively in insulin-producing beta-cells, and two linkage disequilibrium blocks that contain genes potentially involved in beta-cell development or function (IDE-KIF11-HHEX and EXT2-ALX4). These associations explain a substantial portion of disease risk and constitute proof of principle for the genome-wide approach to the elucidation of complex genetic traits.

0 comments Cited 759 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The neurobiology of zinc in health and disease.

Christopher Frederickson, Jae-Young Koh, Ashley Bush (2005)

The use of zinc in medicinal skin cream was mentioned in Egyptian papyri from 2000 BC (for example, the Smith Papyrus), and zinc has apparently been used fairly steadily throughout Roman and modern times (for example, as the American lotion named for its zinc ore, 'Calamine'). It is, therefore, somewhat ironic that zinc is a relatively late addition to the pantheon of signal ions in biology and medicine. However, the number of biological functions, health implications and pharmacological targets that are emerging for zinc indicate that it might turn out to be 'the calcium of the twenty-first century'.

0 comments Cited 355 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

T(H)-17 cells in the circle of immunity and autoimmunity.

Estelle Bettelli, Mohamed Oukka, Vijay K. Kuchroo (2007)

CD4(+) effector T cells have been categorized into two subsets: T helper type 1 (T(H)1) and T(H)2. Another subset of T cells that produce interleukin 17 (IL-17; 'T(H)-17 cells') has been identified that is highly proinflammatory and induces severe autoimmunity. Whereas IL-23 serves to expand previously differentiated T(H)-17 cell populations, IL-6 and transforming growth factor-beta (TGF-beta) induce the differentiation of T(H)-17 cells from naive precursors. These data suggest a dichotomy between CD4(+) regulatory T cells positive for the transcription factor Foxp3 and T(H)-17 cells: TGF-beta induces Foxp3 and generates induced regulatory T cells, whereas IL-6 inhibits TGF-beta-driven Foxp3 expression and together with TGF-beta induces T(H)-17 cells. Emerging data regarding T(H)-17 cells suggest a very important function for this T cell subset in immunity and disease.

0 comments Cited 329 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

: hirano@molonc.med.osaka-u.ac.jp

Journal

Journal ID (nlm-ta): J Biol Inorg Chem

Title: Journal of Biological Inorganic Chemistry

Publisher: Springer-Verlag (Berlin/Heidelberg )

ISSN (Print): 0949-8257

ISSN (Electronic): 1432-1327

Publication date (Electronic): 10 June 2011

Publication date PMC-release: 10 June 2011

Publication date (Print): October 2011

Volume: 16

Issue: 7

Pages: 1123-1134

Affiliations

[1 ]Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Kanagawa 230-0045 Japan

[2 ]Laboratory of Allergy and Immunology, Graduate School of Medicine, Osaka University, Osaka, 565-0871 Japan

[3 ]Immune System, Cooperation Program, Graduate School of Frontier Biosciences, Osaka University, Osaka, 565-0871 Japan

[4 ]Laboratories of Developmental Immunology, JST-CREST, Graduate School of Frontier Biosciences, Graduate School of Medicine, WPI Immunology Frontier Research Center, Osaka University, Osaka, 565-0871 Japan