Publications by authors named "R E Dempski"

Zn transport across neuronal membranes relies on two classes of transition metal transporters: the ZnT (SLC30) and ZIP (SLC39) families. These proteins function to decrease and increase cytosolic Zn levels, respectively. Dysfunction of ZnT and ZIP transporters can alter intracellular Zn levels resulting in deleterious effects.

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Article Synopsis
  • Cation conducting channelrhodopsins (ChRs) are used in optogenetics to control cell activity with light, but understanding their ion transport mechanisms is still incomplete.
  • Researchers studied the C1C2 channelrhodopsin, discovering that a specific mutation (N297D) increased calcium ion (Ca2+) permeability compared to sodium ions (Na+).
  • They used experimental and computational methods to reveal that ion transport involves a unique "swinging" mechanism and identified specific binding sites that influence ion selectivity in the channel.
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The SLC39 family of transporters, otherwise known as ZIPs for Zrt and Irt-like Proteins, function to increase cytosolic levels of transition metals. ZIP transporters have been identified at all phylogenetic levels and are members of the SoLute Carrier (SLC) superfamily. There are fourteen ZIP transporters encoded in the human genome.

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  • The human ZIP4 (hZIP4) is a transporter that helps increase zinc levels in cells and has a structure featuring eight transmembrane domains and a large extracellular domain (ECD).
  • When cells lack zinc, the ECD is cleaved, and mutations in this ECD can lead to a zinc-deficiency disease known as Acrodermatitis enteropathica.
  • Research using Fluorescence Correlation Spectroscopy (FCS) shows that both full-length hZIP4 and a version without the ECD form dimers in cells, indicating the importance of the ECD in understanding hZIP4's function and its role in related diseases.
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The human (h) transporter hZIP4 is the primary Zn importer in the intestine. hZIP4 is also expressed in a variety of organs such as the pancreas and brain. Dysfunction of hZIP4 can result in the Zn deficiency disease acrodermatitis enteropathica (AE).

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