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ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Research » Publications at this Location » Publication #146672
Title: EFFLUX AND COMPARTMENTALIZATION OF ZINC BY MEMBERS OF THE SLC30 FAMILY OF SOLUTE CARRIERS

Author
item PALMITER, RICHARD - UNIVERSITY OF WASHINGTON
item Huang, Liping

Submitted to: Journal of Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/14/2003
Publication Date: 5/14/2003
Citation: Palmiter, R.D., Huang, L. 2004. Efflux and compartmentalization of zinc by members of the slc30 family of solute carriers. Journal of Physiology (2004) 447:744-51.

Interpretive Summary: Zinc is an essential trace element required for the function of many zinc-containing proteins. In mammal, zinc is absorbed through the brush border of small intestinal mucosa from diet and transported through blood to the tissues and cells where zinc is needed. Two families of zinc transporter proteins, ZIP (ZRT1, IRT1-like protein, SLC39) and ZnT (Zinc Transporter, SLC30) are thought to facilitate in zinc uptake, storage, and export. The ZIP proteins appear to function in uptake of zinc into the cytoplasm and in transport of zinc out of intracellular compartments while the cytoplasmic/nuclear zinc is low. The ZnT proteins appear to function in transport of zinc out of cells or in sequestration of zinc into various intracellular compartments while the cytoplasmic/nuclear zinc is high or zinc is needed in the secretory fluids. Thus, ZnT transporters are thought to help maintain zinc homeostasis and facilitate transport of zinc into specialized intracellular compartments. Counterparts of SLC30 family are found in all organisms. Most of the members of this class are predicted to have 6 transmembrane domains with both N- and C-termini on the cytoplasmic side of the membrane. Expression of rodent Znt1, Znt2 or Znt4 cDNAs in mammalian cells can confer resistance to zinc toxicity. Loss of function of the mouse Znt1 is embryonic lethal, loss of mouse Znt3 prevents accumulation of zinc in synaptic vesicles, nonfunctional mouse Znt4 (lethal milk) results in zinc-deficient milk, and Znt5-null mice display bone abnormalities and heart failure. No mutations in human counterparts of any of the members of the SLC30 family have been described.

Technical Abstract: All of the members of this family are thought to facilitate zinc efflux from the cytoplasm either into various intracellular compartments (endosomes, secretory granules, synaptic vesicles, Golgi apparatus, or trans-Golgi network) or across the plasma membrane. Thus, these transporters are thought to help maintain zinc homeostasis and facilitate transport of zinc into specialized intracellular compartments. Counterparts of SLC30 family are found in all organisms. Most of the members of this class are predicted to have 6 transmembrane domains with both N- and C-termini on the cytoplasmic side of the membrane. Expression of rodent Znt1, Znt2 or Znt4 cDNAs in mammalian cells can confer resistance to zinc toxicity. Loss of function of the mouse Znt1 is embryonic lethal, loss of mouse Znt3 prevents accumulation of zinc in synaptic vesicles, nonfunctional mouse Znt4 (lethal milk) results in zinc deficient milk, and Znt5-null mice display bone abnormalities and heart failure. No mutations in human counterparts of any of the members of the SLC30 family have been described.