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SLC39A1 Membrane Protein Introduction

Introduction of SLC39A1

SLC39A1, also known as ZIP1, belongs to the SLC39 family that regulates zinc levels. It is expressed widely in mammalian tissues and cells, in both plasma membrane and intracellular vesicles. Specifically, it is the major zinc uptake transporter in K562 erythroleukemia cells and prostate cells, where it is localized to the plasma membrane. Its expression appears to be regulated by zinc status and by hormone treatment. Interestingly, when cells are cultured by zinc-replete media, ZIP1 is mainly present in intracellular organelles, while when zinc is limiting it translocates to the cell surface. Zinc uptake by ZIP has been found to be energy independent, stimulated by HCO3-. Structurally, it has eight predicted transmembrane domains. The functions of ZIP1 can be inhibited by Ni2+ ions but not Fe2+ ions.

Basic Information of SLC39A1
Protein Name Zinc transporter ZIP1
Gene Name SLC39A1
Aliases Solute carrier family 39 member 1, Zinc-iron-regulated transporter-like, Zrt- and Irt-like protein 1, IRT1, ZIP1, ZIRTL
Organism Homo sapiens (Human)
UniProt ID Q9NY26
Transmembrane Times 8
Length (aa) 324
Sequence MGPWGEPELLVWRPEAVASEPPVPVGLEVKLGALVLLLVLTLLCSLVPICVLRRPGANHEGSASRQKALSLVSCFAGGVFLATCLLDLLPDYLAAIDEALAALHVTLQFPLQEFILAMGFFLVLVMEQITLAYKEQSGPSPLEETRALLGTVNGGPQHWHDGPGVPQASGAPATPSALRACVLVFSLALHSVFEGLAVGLQRDRARAMELCLALLLHKGILAVSLSLRLLQSHLRAQVVAGCGILFSCMTPLGIGLGAALAESAGPLHQLAQSVLEGMAAGTFLYITFLEILPQELASSEQRILKVILLLAGFALLTGLLFIQI

Functions of SLC39A1 Membrane Protein

SLC39A1, a major regulator of prostate gland zinc, is responsible for the rapid uptake and accumulation of zinc in prostate cells. The down-regulation of SLC39A1 transporter decreases zinc to prevent its cytotoxic effects. Reduced accumulation of zinc in tumorigenic prostate epithelial cells might be partly due to the decreased expression or deficiency of SLC39A1 protein. As a result, studies have reported SLC39A1 has a role of tumor suppression in the prostate, and that zinc treatment approach has been proposed for prostate cancer treatment, using ionophore such as clioquinol.

SLC39A1 Membrane Protein Introduction

Application of SLC39A1 Membrane Protein in Literature

  1. Chen X., et al. Phosphorylation of the synaptonemal complex protein Zip1 regulates the crossover/noncrossover decision during yeast meiosis. PLoS biology. 2015, 13(12): e1002329. PubMed ID: 26682552

    This study identified a conserved region on the C terminus of the Zip1 transporter, and the phosphorylation of which was required for the crossover formation during yeast meiosis.

  2. Xu S., et al. ZIP1 and zinc inhibits fluoride-induced apoptosis in MC3T3-E1 cells. Biological trace element research. 2014, 159(1-3): 399-409. PubMed ID: 24752969

    This study investigated the effects of zinc and ZIP1 on fluoride-induced apoptosis in mouse MC3T3-E1 cells as well as the underlying molecular mechanisms. The results showed that treatment with zinc significantly attenuated the apoptosis induced by fluoride and that overexpression of ZIP1 inhibited this process as well.

  3. Costello L.C., et al. Evidence that human prostate cancer is a ZIP1-deficient malignancy that could be effectively treated with a zinc ionophore (Clioquinol) approach. Chemotherapy. 2015, 4(2). PubMed ID: 26273543

    This article reviewed the studies that used the zinc ionophore (Clioquinol) approach for the treatment of human prostate cancer, providing strong support for this treatment approach that should be pursued with additional research.

  4. Furuta T., et al. Oxidative stress upregulates zinc uptake activity via Zrt/Irt-like protein 1 (ZIP1) in cultured mouse astrocytes. Life sciences. 2016, 151: 305-312. PubMed ID: 26979775

    To investigate whether the functionality of the zinc clearance system was altered under oxidative stress-loaded conditions, this study characterized zinc uptake by oxidative stress-loaded astrocytes using mouse astrocytes. The results indicated that the increased zinc clearance activity of astrocytes under oxidative stress-loaded conditions might be due to increased ZIP1 expression.

  5. Liu X.W., et al. Melatonin exerts protective effect on N2a cells under hypoxia conditions through Zip1/ERK pathway. Neuroscience letters. 2015, 595: 74-80. PubMed ID: 25864781

    This study investigated the effects of melatonin in hypoxia-induced N2a cells and the results showed that melatonin activated the MAPK/ERK pathway via upregulating the expression of Zip1.

SLC39A1 Preparation Options

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