SLC30A10 Membrane Protein Introduction

Introduction of SLC30A10

Solute carrier family 30 member 10 (SLC30A10), also known as zinc transporter 10 (ZnT-10) or manganese transporter SLC30A10, is a protein that in humans is encoded by the SLC30A10 gene. It is a member of the SLC30 proteins that belong to the cation diffusion facilitator (CDF) superfamily of metal transporters.

Function of SLC30A10 Membrane Protein

SLC30A10 or ZnT-10 is a member of the SLC30 family proteins. Unlike most of the SLC30 members that transport zinc, SLC30A10 appears to be critical in maintaining manganese levels and has higher specificity for manganese than zinc. The expression of SLC30A10 is predominantly found in the human liver, brain, testis, and small intestine. It has been reported that the wild-type (WT) SLC30A10 protein could act as a cell surface-localized manganese efflux transporter that reduces intracellular manganese levels and protects against manganese toxicity. Furthermore, loss of function mutations appears to result in a pleomorphic phenotype, including dystonia and adult-onset parkinsonism. Studies have shown that SLC30A10 is associated with neurodegenerative diseases. Recently, the decrease of SLC30A10 level is found in the brain of Alzheimer's disease (AD) patients.

Fig.1 Model for transporter activity for mammalian manganese absorption, hepatic uptake, and endogenous excretion. (Aydemir, 2017)

Application SLC30A10 of Membrane Protein in Literature

1. Zogzas C.E. and Mukhopadhyay S. Putative metal binding site in the transmembrane domain of the manganese transporter SLC30A10 is different from that of related zinc transporters. Metallomics. 2018, 10(8):1053-1064. PubMed ID: 29989630
   
   

   This research is conducted to resolve the divergent results about the requirement of the crucial asparagine-43 residue. It indicates that the mechanisms of ion coordination within the transmembrane domain of SLC30A10 substantially differ from previously-studied CDFs, suggesting that factors beyond site A residues may confer metal specificity to CDFs, and improve understanding of the pathobiology of manganese toxicity due to mutations in SLC30A10.

2. Go S., et al. Protective function of SLC30A10 induced via PERK-ATF4 pathway against 1-methyl-4-phenylpyridinium. Biochemical and biophysical research communications. 2017, 490(4):1307-13. PubMed ID: 28688763
   
   

   This article investigates the role of SLC30A10 in the 1-methyl-4-phenylpiridium ion (MPP+)-induced intracellular stress, and the molecular mechanism underlying SLC30A10 induction by MPP+ treatment. It suggests that SLC30A10 has a protective role for MPP+-induced toxicity via PERK-ATF4 pathway.

3. Hutchens S., et al. Deficiency in the manganese efflux transporter SLC30A10 induces severe hypothyroidism in mice. Journal of Biological Chemistry. 2017, 292(23):9760-9773. PubMed ID: 28461334
   
   

   This report finds that thyroid dysfunction plays a key role in the onset and progression of the manganese-induced disease and Slc30a10 knock-out mice can be used as a new model for studying thyroid biology.

4. da Silva T.C., et al. Vitamin D3 transactivates the zinc and manganese transporter SLC30A10 via the Vitamin D receptor. The Journal of steroid biochemistry and molecular biology. 2016, 163:77-87. PubMed ID: 27107558
   
   

   This article demonstrates that vitamin D3 transactivates the SLC30A10 gene in a VDR-dependent manner, resulting in increased ZnT10 protein expression.

5. Zogzas C.E., et al. Structural elements in the transmembrane and cytoplasmic domains of the metal transporter SLC30A10 are required for its manganese efflux activity. Journal of Biological Chemistry. 2016, 291(31):15940-57. PubMed ID: 27307044
   
   

   This article indicates that residues in the transmembrane and C-terminal domains together confer optimal manganese transport capability to SLC30A10 and suggests that the mechanism of ion coordination in the transmembrane domain of SLC30A10 may be substantially different from that in YiiP/other SLC30 proteins.

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Reference

1. Aydemir, et al. (2017). Metal transporter Zip14 (Slc39a14) deletion in mice increases manganese deposition and produces neurotoxic signatures and diminished motor activity. Journal of Neuroscience. 37(25): 5996-6006.

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