SLC16A1 Membrane Protein Introduction

Introduction of SLC16A1

SLC16A1 is also known as Monocarboxylate transporter 1 or Solute carrier family 16 member 1. It belongs to the proton-linked monocarboxylate transporter (MCT) family which is responsible for the proton-linked transport of important monocarboxylate metabolites, such as pyruvate, L-lactate and the ketone bodies and plays a central role in cellular metabolism and metabolic communication between tissues. All family members are predicted to have 12-transmembrane helices (TMs) with intracellular C- and N-termini and a large cytosolic loop between TMs 6 and 7.

Function of SLC16A1 Membrane Protein

SLC16A1 was first characterized extensively using classical radiotracer techniques in red blood cells and the molecular mechanism of SLC16A1 has been extensively studied. The activity of SLC16A1 is enhanced by interaction with intracellular carbonic anhydrase II whilst that of MCT2 is stimulated by interaction with extracellular carbonic anhydrase IV. In skeletal muscle, numerous studies have shown up-regulation of SLC16A1 in response to chronic stimulation or exercise in rats and humans, whilst down-regulation occurs in response to denervation or spinal injury. SLC16A1 may also be involved in the activation of gene expression mediated by AMP-activated protein kinase (AMPK). AMP increases in response to exercise and the SLC16A1 promoter has been shown to be stimulated following AMPK activation. The SLC16A1 promoter has several consensus NFAT binding sequences which are known to be important in the activation and proliferation of T-lymphocytes, a process also accompanied by a large (several-fold) increase in SLC16A1 expression to support greatly stimulated rates of glycolysis.

Fig.1 Proposed mechanisms of SLC16A1. (Filippi, 2008)

Application of SLC16A1 Membrane Protein in Literature

1. Halestrap A.P. The SLC16 gene family – Structure, role and regulation in health and disease. Molecular Aspects of Medicine. 2013, 34(2):337-349. PubMed ID: 23506875
   
   

   This article reports that potent SLC16A1-specific inhibitors will provide a valuable tool for investigating the metabolic roles of SLC16A1, and their ability to act as immunosuppressive drugs illustrates the promise of MCTs as pharmacological targets.

2. Al-mosauwi H., et al. Differential protein abundance of a basolateral MCT1 transporter in the human gastrointestinal tract. Cell Biol. Int. 2016, 40(12):1303-1312. PubMed ID: 27634412
   
   

   This article reveals that basolateral SLC16A1 protein abundance is correlated to levels of bacterially derived SCFAs along the human gastrointestinal tract. These findings highlight the importance of precise tissue location in studies comparing colonic SLC16A1 abundance between normal and diseased states.

3. Petersen C., et al. MCT1 and MCT4 Expression and Lactate Flux Activity Increase During White and Brown Adipogenesis and Impact Adipocyte Metabolism. Scientific Reports. 2017, 7(1):13101. PubMed ID: 29026134
   
   

   This article suggests that SLC16A1 and MCT4, as well as NBCe1, are strongly upregulated at the mRNA and protein level upon adipocyte differentiation for the first time. The differentiation was accompanied by enhanced lactate flux capacity, which was strongly reduced by SLC16A1 inhibition and SLC16A1 knockdown.

4. Majumdar S., et al. Functional Activity of a Monocarboxylate Transporter, MCT1, in the Human Retinal Pigmented Epithelium Cell Line, ARPE-19. Mol. Pharm. 2005, 2(2):109-117. PubMed ID: 15804185
   
   

   The results of this article indicate that SLC16A1 is functionally active and is the only MCT isoform involved in the apical uptake of monocarboxylates by ARPE-19 cells.

5. Sasa K., et al. Monocarboxylate transporter-1 promotes osteoblast differentiation via suppression of p53, a negative regulator of osteoblast differentiation. Scientific Reports. 2018, 8:10579. PubMed ID: 30002387
   
   

   The article shows that MCT-1 functions as a positive regulator of osteoblast differentiation via suppression of p53 because MCT-1 facilitates osteoblast differentiation via suppression of p53 expression and activation.

SLC16A1 Preparation Options

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Reference

1. Filippi BM & Alessi DR. (2008) Novel role for the LKB1 pathway in controlling monocarboxylate fuel transporters. The Journal of Cell Biology. 183(1):7.

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