SLC16A11 Membrane Protein Introduction

Introduction of SLC16A11

SLC16A11 is also known as Monocarboxylate transporter 11, MCT 11, Solute carrier family 16 member 11. It is a member of the SLC16 (or monocarboxylate transporter, MCT) family, a group of 14 solute carriers that is defined by two highly conserved sequences. Three-dimensional homology modeling of SLC16A11 based on the solved structure of the bacterial glycerol 3 phosphate transporter (GlPT) suggests that SLC16A11 belongs to category I and it might transport monocarboxylates via a H^⁺-coupled mechanism.

Function of SLC16A11 Membrane Protein

SLC16A11 is expressed in relatively few tissues, with the highest levels detected in thyroid, liver, and salivary gland, however, the role of SLC16A11 in these tissues has not been characterized very clearly yet. The structural analyses according to the Three-dimensional homology modeling of SLC16A11 based on the solved structure of the bacterial glycerol-3-phosphate transporter (GlPT) suggest that SLC16A11 belongs to category I, and it might transport monocarboxylates via an H^⁺-coupled mechanism. Some (presumably, non-coding regulatory) variants on the Type 2 Diabetes risk haplotype lead to decreased gene expression of SLC16A11 in liver, while coding variants affect the interaction of the SLC16A11 protein with basigin leading to reduced levels of the transporter at the cell surface. More importantly, disruption of SLC16A11 in primary human hepatocytes leads to T2D-relevant changes in fatty acid and lipid metabolism. Reduced SLC16A11 that functions in liver might be a causal factor for Type 2 Diabetes, suggesting that SLC16A11 might be a novel therapeutic target.

Fig.1 Proposed signaling pathway of SLC16A11 in Type 2 Diabetes. (Rusu, 2017)

Application of SLC16A11 Membrane Protein in Literature

1. Rusu V., et al. Type 2 diabetes variants disrupt function of SLC16A11 through two distinct mechanisms. Cell. 2017, 170(1):199-212.e120. PubMed ID: 28666119
   
   

   The results of this article demonstrate that SLC16A11 is a proton-coupled monocarboxylate transporter, and that genetic perturbation of SLC16A11 induces changes in fatty acid and lipid metabolism that are associated with increased Type 2 Diabetes risk. The findings suggest that increasing SLC16A11 function could be therapeutically beneficial for Type 2 Diabetes.

2. The STDC. (2014) Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico. Nature. 2014, 506(7486):97-101. PubMed ID: 24390345
   
   

   Authors in this group apply genetic studies in multiple human populations to identify SLC16A11 as a novel candidate gene for Type 2 Diabetes with a possible role in triacylglycerol metabolism.

3. Miranda-Lora América L., et al. Associations of common variants in the SLC16A11, TCF7L2, and ABCA1 genes with pediatric-onset type 2 diabetes and related glycemic traits in families: A case-control and case-parent trio study. Pediatric Diabetes. 2017, 18(8):824-831. PubMed ID: 28101933
   
   

   This article indicates that SLC16A1 /rs13342232 might be involved in the risk of pediatric-onset Type 2 Diabetes in Mexican families because the G allele of SLC16A1 /rs13342232 was associated with Type 2 Diabetes in adults.

4. Traurig M., et al. Analysis of SLC16A11 Variants in 12,811 American Indians: Genotype-Obesity Interaction for Type 2 Diabetes and an Association With RNASEK Expression. Diabetes. 2016, 65(2):510-519. PubMed ID: 26487785
   
   

   The authors in this article analyze SLC16A11 in 12,811 North American Indians and found that the diabetes risk haplotype, tagged by the rs75493593 A allele, was nominally associated with type 2 diabetes.

5. Lara-Riegos J.C., et al. Diabetes susceptibility in Mayas: Evidence for the involvement of polymorphisms in HHEX, HNF4α, KCNJ11, PPARγ, CDKN2A/2B, SLC30A8, CDC123/CAMK1D, TCF7L2, ABCA1 and SLC16A11 genes. Gene. 2015, 565(1):68-75. PubMed ID: 25839936
   
   

   This article suggests that ABCA1 and SLC16A11 are related mainly to impaired metabolic traits and consequently involved in type 2 diabetes susceptibility.

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Reference

1. Rusu V., et al. (2017) Type 2 diabetes variants disrupt function of SLC16A11 through two distinct mechanisms. Cell. 170(1):199-212.e120.

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