SLC39A2 Membrane Protein Introduction

Introduction of SLC39A2

SLC38A2, also called ZIP2, belongs to the subfamily II of SLC39A family of zinc transporters. It is a zinc uptake transporter. SLC38A2-mediated transport is modulated by extracellular pH, with an H+ driving-force independent and voltage-dependent manner. In addition to zinc, SLC38A2 also mediates the uptake of Cd2+ in a pH-dependent manner, which is inhibited by extracellular Zn2+, Cu2+, and to a lesser extent Co2+, but not by Mn2+ or Ba2+. Fe2+ is not transported by SLC38A2. The substrate selectivity of SLC38A2 decreases in the following order: Zn2+ > Cd2+ > Cu2+ > Co2+. This transporter is widely distributed and the expression is modulated by zinc. Especially, it is expressed in prostate and uterine epithelial cells. structurally, it is predicted to have 8 transmembrane-spanning domains, with both N-terminus and C-terminus facing the extracellular side.

Basic Information of SLC39A2
Protein Name Zinc transporter ZIP2
Gene Name SLC39A2
Aliases 6A1, Eti-1, Solute carrier family 39 member 2, Zrt- and Irt-like protein 2, ZIP2
Organism Homo sapiens (Human)
UniProt ID Q9NP94
Transmembrane Times 8
Length (aa) 309

Functions of SLC39A2 Membrane Protein

SLC39A2 may be important in the contact inhibition of normal epithelial cells. Moreover, although the targeted disruption of the ZIP1, ZIP2, or ZIP3 alleles does not produce any obvious embryonic phenotype under normal dietary conditions, abnormal embryonic development in mice can be observed under limiting Zn intake conditions during pregnancy. This suggested that deficiency of these genes rendered the animal more sensitive to Zn deficiency during pregnancy. Besides, SLC38A2 is involved in the development of prostate cancer. Studies have revealed that SLC38A2 is downregulated in prostate cancer, whereas it is abundantly present in normal prostate epithelial cells and in benign prostate hyperplasia (BPH).

SLC39A2 Membrane Protein Introduction

Application of SLC39A2 Membrane Protein in Literature

  1. Kamei S., et al. Zinc deficiency via a splice switch in zinc importer ZIP2/SLC39A2 causes cystic fibrosis-associated MUC5AC hypersecretion in airway epithelial cells. EBioMedicine. 2018, 27: 304-316. PubMed ID: 29289532

    This study demonstrated that zinc deficiency via the unique slicing switch in zinc importer ZIP2 is crucial for cystic fibrosis (CF), especially the induction of MUC5AC, a major secreted mucin that is highly expressed in CF airway.

  2. Franz M.C., et al. Reassessment of the transport mechanism of the human zinc transporter SLC39A2. Biochemistry. 2018, 57(26): 3976-3986. PubMed ID: 29791142

    This article reassessed the transport mechanism of the human zinc transporter ZIP2, in terms of pH sensitivity, transport inhibition, substrate specificity, transport kinetics, etc.

  3. Giacconi R., et al. Effect of ZIP2 Gln/Arg/Leu (rs2234632) polymorphism on zinc homeostasis and inflammatory response following zinc supplementation. Biofactors. 2015, 41(6): 414-423. PubMed ID: 26643924

    This study investigated the role of ZIP2 SNP on zinc and inflammatory status in elderly healthy free-living subjects, and inflammatory responses to zinc supplementation.

  4. Inoue Y., et al. ZIP2, a zinc transporter, is associated with keratinocyte differentiation. Journal of Biological Chemistry. 2014, 289(31): 21451-62. 560821. PubMed ID: 24936057

    This study investigated the ZIP proteins specifically expressed in the epidermis and their functions. The findings showed that ZIP2 are necessary for keratinocyte differentiation.

  5. Tao Y., et al. Up-regulation of Slc39A2 (Zip2) mRNA in peripheral blood mononuclear cells from patients with pulmonary tuberculosis. Molecular biology reports. 2013, 40(8): 4979-4984. PubMed ID: 23686108

    This study investigated whether Zip2 level was changed in the patients with pulmonary tuberculosis (PTB). The data showed that increased expression of Zip2 gene is closely associated with the immunity of PTB patients.

SLC39A2 Preparation Options

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