IMR Press / FBL / Volume 22 / Issue 8 / DOI: 10.2741/4546

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


The mucolipin-1 (TRPML1) ion channel, transmembrane-163 (TMEM163) protein, and lysosomal zinc handling

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1 Department of Biological Science, California State University Fullerton, Fullerton, CA, 92831, USA
2 Center for Applied Biotechnology Studies, California State University Fullerton, Fullerton, CA, 92831, USA
3 Department of Biological Sciences, University of Pittsburgh, PA, 15260, USA

Academic Editors: Hui-Ling Chiang, Shannon Kelleher

Front. Biosci. (Landmark Ed) 2017, 22(8), 1330–1343;
Published: 1 March 2017
(This article belongs to the Special Issue Membrane transport)

Lysosomes are emerging as important players in cellular zinc ion (Zn2+) homeostasis. The series of work on Zn2+ accumulation in the neuronal lysosomes and the mounting evidence on the role of lysosomal Zn2+ in cell death during mammary gland involution set a biological precedent for the central role of the lysosomes in cellular Zn2+ handling. Such a role appears to involve cytoprotection on the one hand, and cell death on the other. The recent series of work began to identify the molecular determinants of the lysosomal Zn2+ handling. In addition to zinc transporters (ZnT) of the solute-carrier family type 30A (SLC30A), the lysosomal ion channel TRPML1 and the poorly understood novel transporter TMEM163 have been shown to play a role in the Zn2+ uptake by the lysosomes. In this review, e summarize the current knowledge on molecular determinants of the lysosomal Zn2+ handling, uptake, and release pathways, as well as discuss their possible roles in health and disease.

Mucolipidosis IV
zinc transport
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