SLC39A3 Membrane Protein Introduction

Introduction of SLC39A3

Zinc transporter ZIP3 (short for ZIP-3), alternatively called the Zrt- and Irt-like protein 3, is encoded by the SLC39A3 gene in human. The zinc transporter SLC39A3 is a member of the ZIP family, also known as solute carrier family 39 (SLC39) that transport Zn²⁺ across the membrane into the cytosol, either from the lumen of intracellular organelles or from the extracellular space. Zinc transporter SLC39A3 is broadly expressed in testis, brain and other tissues at similar levels. Within the central nervous system, SLC39A3 is abundantly expressed in the spinal cord, cortex, thalamus, and the retina.

Function of SLC39A3 Membrane Protein

Zinc transporters, or zinc transporter proteins (Zrt), are membrane transport proteins of the solute carrier family that modulate the membrane transport of zinc and regulate its intracellular and cytoplasmic concentrations. They consist of two main groups: the zinc importer, Zrt- and Irt-like protein (ZIP), or solute carrier 39A (SLC39A) family and the zinc transporter (ZnT) or solute carrier 30 (SLC30) family. The SLC39A family comprises 14 members which are supposed to control the cytosolic concentration of zinc by transporting zinc into the cytoplasm from the extracellular space or from intracellular compartments. Zinc transporter SLC39A3 shows several biochemical functions, including zinc ion transmembrane transporter activity. SLC39A3 forms dimers with SLC39A 1-3, and interacts with PKC-ζ and the shaker-type potassium channel subunit Kvβ2. Human SLC39A3 seems to contribute to the re-uptake and conservation of zinc from the prostatic fluid. A study has proposed that zinc is a tumor-suppressor agent and SLC39A3 is a tumor suppressor gene in prostate cancer.

Fig.1 Predicted structure of the zinc transporters ZIP and ZnT. (Norouz, 2017)

Application of SLC39A3 Membrane Protein in Literature

1. Hennigar S.R., et al. Metallothionein and Zinc Transporter Expression in Circulating Human Blood Cells as Biomarkers of Zinc Status: a Systematic Review. Adv Nutr. 2016, 7(4): 735-46. PubMed ID: 27422508
   
   

   Authors in this study attempted to compile and assess studies that determined zinc transporter and/or metallothionein expression in various blood cell types and to determine their reliability and sensitivity to changes in dietary zinc.

2. Schweigel-Röntgen M. The families of zinc (SLC30 and SLC39) and copper (SLC31) transporters. Curr Top Membr. 2014, 73: 321-55. PubMed ID: 24745988
   
   

   This article summarized the discovery of zinc transporters, as well as the structure, expression and function of SLC30, SLC39, and SLC31 respectively.

3. Franklin R.B., et al. The cytotoxic role of RREB1, ZIP3 zinc transporter, and zinc in human pancreatic adenocarcinoma. Cancer Biol Ther. 2014, 15(10): 1431-7. PubMed ID: 25050557
   
   

   The results of this study further demonstrated that ZIP3 was the important transporter required for the accumulation of zinc and its inhibition of proliferation.

4. Costello L.C., et al. Evidence for changes in RREB-1, ZIP3, and Zinc in the early development of pancreatic adenocarcinoma. J Gastrointest Cancer. 2012, 43(4): 570-8. PubMed ID: 22427155
   
   

   Authors of this study showed that zinc, ZIP3, and RREB-1 were markedly decreased in early-stage adenocarcinoma, which indicated a new concept of early genetic/metabolic events in the progressive transformation of normal cells to premalignant cells in the development of pancreatic cancer.

5. Costello L.C., et al. Decreased zinc and downregulation of ZIP3 zinc uptake transporter in the development of pancreatic adenocarcinoma. Cancer Biol Ther. 2011, 12(4): 297-303. PubMed ID: 21613827
   
   

   The findings of this article suggested that the combination of concurrent zinc, ZIP3, and RREB-1 changed represent early events in the development of adenocarcinoma.

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Reference

1. Norouzi S, et al. (2017). Zinc transporters and insulin resistance: therapeutic implications for type 2 diabetes and metabolic disease.Journal of biomedical science. 24(1): 87.

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