SLC16A10 Membrane Protein Introduction

Introduction of SLC16A10

SLC16A10 is also known as Monocarboxylate transporter 10, Aromatic amino acid transporter 1, Solute carrier family 16 member 10, and T-type amino acid transporter 1. It belongs to the Monocarboxylate transporter family which catalyzes the proton-linked transport of monocarboxylates such as L-lactate across the plasma membrane, whereas MCT8 and SLC16A10 are thyroid hormone and aromatic amino acid transporters, respectively. SLC16A10 is a highly related thyroid hormone transport protein which is also known as TAT1 or T-type amino acid transporter.

Function of SLC16A10 Membrane Protein

SLC16A10 is discovered by expression cloning in Xenopus oocytes and shown to transport aromatic amino acids (phenylalanine, tyrosine, and tryptophan) in a sodium and proton independent manner with Km values of about 1 mM. Two highly homologous monocarboxylate transporters, MCT8 and SLC16A10, are so far the only identified transporters with high activity and specificity for thyroid hormone. SLC16A10 facilitate not only the cellular uptake but also the efflux of thyroid hormone from cells. Overexpression of SLC16A10 on the TRb1 mediated stimulation of a TRE driven luciferase reporter by triiodothyronine in JEG3 human choriocarcinoma cells, which show low endogenous expression of thyroid hormone transporters. Overexpression of SLC16A10 stimulates triiodothyronine uptake, resulting in a rapid rise in intracellular triiodothyronine concentration. Apart from thyroid hormone, SLC16A10 is also capable of transporting aromatic amino acids. SLC16A10 functions as a net efflux pathway for aromatic amino acids in the basosolateral epithelial cells.

Fig.1 The role of SLC16A10 in thyroid hormone signaling pathway. (Préau, 2015)

Application of SLC16A10 Membrane Protein in Literature

1. Préau L., et al. Thyroid hormone signaling during early neurogenesis and its significance as a vulnerable window for endocrine disruption. Biochim. Biophys. Acta. 2015, 1849(2):112-121. PubMed ID: 24980696
   
   

   This article reports that the best characterized monocarboxylase transporters 8 (MCT8) and 10 (SLC16A10) play important roles in regulating the thyroid hormone signaling pathway.

2. van Mullem A.A., et al. Effects of thyroid hormone transporters MCT8 and MCT10 on nuclear activity of T3. Mol. Cell. Endocrinol. 2016, 437:252-260. PubMed ID: 27492966
   
   

   This article reveals that MCT8 and SLC16A10 increase the availability of triiodothyronine for its nuclear receptor rather than generate a rapid equilibrium between cellular and serum triiodothyronine.

3. Sharlin D.S., et al. Deafness and loss of cochlear hair cells in the absence of thyroid hormone transporters Slc16a2 (Mct8) and Slc16a10 (Mct10). Scientific Reports. 2018, 8:4403. PubMed ID: 29535325
   
   

   The results of this article demonstrate a key role for SLC16A2 (MCT8) and SLC16A10 transporters in the development of hearing and maintenance of cochlear structure. The findings suggest that apart from the systemic provision of thyroid hormone, cellular uptake or efflux of the hormone by transmembrane transporters is required to promote cochlear development and hearing.

4. Uemura S., et al. Functional analysis of human aromatic amino acid transporter MCT10/TAT1 using the yeast Saccharomyces cerevisiae. Biochim. Biophys. Acta. 2017, 1859(10):2076-2085. PubMed ID: 28754537
   
   

   This article shows that human aromatic amino acid transporter SLC16A10 is functional in yeast and mediates low-affinity and pH-independent tryptophan import in yeast, and is subject to ubiquitination. Meanwhile, The N81K mutation in the TMD1 abolishes tryptophan import activity of SLC16A10.

5. Abe S., et al. Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes. Endocrinology. 2012, 153(8):4049-4058. PubMed ID: 22719050
   
   

   These findings suggest that SLC16A10 functions as a thyroid hormone transporter in chondrocytes and can explain at least in part why Allan-Herndon-Dudley syndrome patients do not exhibit significant growth impairment.

SLC16A10 Preparation Options

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Reference

1. Préau L., et al. (2015) Thyroid hormone signaling during early neurogenesis and its significance as a vulnerable window for endocrine disruption. Biochim. Biophys. Acta. 1849(2):112-121.

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