Alzheimer’s Disease: Zinc Transporters May Shed Light on Molecular Mechanism

Alzheimer’s Disease: Zinc Transporters May Shed Light on Molecular Mechanism
Unbalanced, unhealthy zinc levels show in many diseases including Alzheimer's disease, Parkinson's disease, and pancreatic cancer. But lack of information about the molecular structure of zinc transporters hampers the discovery of new drugs to bring zinc to proper levels (homeostasis) with other important elements. Researchers at Michigan State University (MSU) have taken a new step toward the development of such drugs, by providing a crystal structure of the extracellular domain (ECD) of ZIP4, a protein expressed by cells that line the intestine and are involved in the uptake of zinc from food. The study, "Structural insights of ZIP4 extracellular domain critical for optimal zinc transport", was published in Nature Communications. Zinc ion, the second most abundant trace element in humans after iron, is essential in a variety of biological processes and must be tightly regulated. It is required for the proper function of several enzymes in the body, for the activity of proteins that regulate gene expression, and it is thought to act as a neurotransmitter. In mammals, zinc homeostasis is mainly maintained by two zinc transporter families, the ZnT family, responsible for removing zinc from the cells, and the ZIP family which mediates zinc uptake and increases its concentration in the cell cytoplasm. ZIP4 has been shown to be over expressed in several types of cancers, including prostate cancer. Mutations in ZIP4 lead to a rare but lethal genetic disease called ecrodermatitis enteropathica (AE), whic
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