SLC16A6 Membrane Protein Introduction

Introduction of SLC16A6

SLC16A6 is a member of solute carrier family 16, also known as the monocarboxylic acid transporter family (MCT). SLC16A6 is a type of transmembrane transporter widely distributed on mammalian cell membranes. The topology of all MCT family members consists of the N-terminal, C-terminal and 12 transmembrane domains. The size of the loop between TM6 and TM7 varies widely. The longest members are MCT5 and MCT7, with 105 amino acids and 93 amino acids respectively. SLC16A6 is mainly expressed in the brain and pancreas.

Function of SLC16A6 Membrane Protein

The solute carrier family 16 has many biological functions, such as promoting the absorption of nutrients, affecting the metabolic homeostasis, regulating intracellular pH and participating in drug delivery. The cells remove the lactic acids produced by glycolysis mainly by SLC16 proteins. The efflux or influx of lactic acids from different cell types is closely related to the transport activity of SLC16 proteins, which means that the activity of SLC16 proteins can regulate the sugar metabolism of cells. Fermentation and glucose balance suggest that SLC16 proteins play an important role in maintaining the homeostasis of the body environment. In skeletal muscle, the transport of lactic acids and pyruvate is not only related to SLC16A1 and SLC16A3 but also because there are other transport proteins, such as SLC16A4 in mice and SLC16A6 in humans.

Fig.1 Tumour metabolic reprogramming, growth-factor-mediated mitogenic signaling and magnesium. (Federica, 2012)

Application of SLC16A6 Membrane Protein in Literature

1. Farzaneh S., et al. New Ferrocene Compounds as Selective Cyclooxygenase (COX-2) Inhibitors: Design, Synthesis, Cytotoxicity and Enzyme-inhibitory Activity. Anticancer Agents Med Chem. 2018, 18(2): 295-301. PubMed ID: 28971779
   
   

   This article demonstrated that synthesized compounds had mild ability to moderate cytotoxicity against MCT7 and T47D in breast cancer cell lines.

2. Kirat D., et al. Expression and cellular localization of monocarboxylate transporters (MCT2, MCT7, and MCT8) along the cattle gastrointestinal tract. Cell Tissue Res. 2013, 352(3): 585-598. PubMed ID: 23417128
   
   

   At the cellular level, the authors used immunohistochemical methods to study the localized MCT2, MCT7, and MCT8 proteins in the cattle rumen, abomasum, jejunum, and caecum.

3. Kirat D., et al. Effect of pectin feeding on monocarboxylate transporters in rat adrenal gland. J Comp Physiol B. 2010, 180(1): 57-65. PubMed ID: 19578859
   
   

   This article showed a significant increase in the expression levels of MCT1, MCT2, MCT4, MCT5, and MCT7 in pectin-fed rats in comparison with the controls. In addition, immunohistochemistry revealed extended distribution and a distinctive increase of the immunoreactivities of MCT1, MCT2, MCT4, MCT5, and MCT7 in the adrenal cortical zones, besides the increase of the immunoreactive intensity of MCT5 and MCT7 in the adrenal medulla of pectin-fed versus control rats.

4. Lian Ee G C., et al. Localization of members of MCT monocarboxylate transporter family Slc16 in the kidney and regulation during metabolic acidosis. Molecules. 2010, 15(4): 2398-2404. PubMed ID: 20428051
   
   

   The authors revealed that pellitorine, isolated from the roots of Piper nigrum, had strong cytotoxic activities against HL60 and MCT7 cell lines.

5. Castelli M.P., et al. Distribution of monocarboxylate transporters MCT1-MCT8 in rat tissues and human skeletal muscle. Appl Physiol Nutr Metab. 2010, 31(1): 31-39. PubMed ID: 16604139
   
   

   Authors observed a pronounced MCT7 signal in human muscle. In skeletal muscle, as well as other tissues, lactate and pyruvate transport rates may not only involve in MCT1 and -4, as other monocarboxylate transporters were also expressed in the rat (MCT2, -5, -6) and human skeletal muscle (MCT2, -5, -6, -7).

SLC16A6 Preparation Options

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Reference

1. Federica I Wolf. (2000). Magnesium and its transporters in cancer: a novel paradigm in tumour development. Clinical Science. 123(7), 417-427.

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