The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Molecular and genetic features of zinc transporters in physiology and pathogenesis
Abstract
Zinc (Zn) is a vital element. It plays indispensable roles in multifarious cellular processes, affecting the expression and activity of a variety of molecules, including transcription factors, enzymes, adapters, channels, growth factors, and their receptors. A disturbance in Zn homeostasis due to Zn deficiency or an excess of Zn absorption can therefore impair the cellular machinery and exert various influences on physiological programs, such as systemic growth, morphogenetic processes, and immune responses, as well as neuro-sensory and endocrine functions. Thus, Zn imbalance becomes pathogenic in humans. Zn homeostasis is controlled by the coordinated actions of Zn transporters, which are responsible for Zn influx and efflux, and intricately regulate the intracellular and extracellular Zn concentration and distribution. In this review, we describe crucial roles of Zn transporters in biological phenomena, focusing in particular on how Zn transporters contribute to cellular events at the molecular, biochemical, and genetic level, with recent progress uncovering the roles of Zn transporters in physiology and pathogenesis.
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Self-citationZinc biochemistry: From a single zinc enzyme to a key element of life
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Zinc as a Gatekeeper of Immune Function
Wessels, I., Maywald, M., & Rink, L. (2017) · Nutrients · doi:10.3390/nu9121286 · Cited by 747
Biological metals and metal-targeting compounds in major neurodegenerative diseases
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The Functions of Metallothionein and ZIP and ZnT Transporters: An Overview and Perspective
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Metadata
- Authors
- Fukada, T., & Kambe, T.
- Venue
- Metallomics
- Publisher
- Oxford University Press (OUP)
- Published
- 2011
- Volume
- 3
- Issue
- 7
- Pages
- 662
- ISSN
- 1756-5901 (ISSN-L)
- 1756-591X
- OpenAlex
- W1971352570
- Cited by
- 294
- References
- 10
- FWCI
- 21.47
- Type
- journal article
- Language
- en
- Open access
- closed
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