SLC47A2 Membrane Protein Introduction

Introduction of SLC47A2

SLC47A2 encoded by SLC47A2 gene, also known as MATE2, is a member of the MATE (multidrug and toxic compound extrusion) family of transporters. It is responsible for the solute transport and its substrates are diverse including tetraethylammonium (TEA), 1-methyl-4-phenylpyridinium (MPP), cimetidine, N-methyl nicotinamide, metformin, creatinine, guanidine, procainamide, topotecan, estrone sulfate, acyclovir, and ganciclovir. SLC47A2 is primarily expressed in the kidney.

Function of SLC47A2 Membrane Protein

SLC47A2/MATE2 is an organic cation/proton exchanger that plays an important role in the renal elimination of toxic electrolytes including endogenous and exogenous, through urine and bile. Its substrates are diverse including many cationic drugs and endogenous compounds. Many studies have indicated that SLC47A2 plays an important role in metformin (a drug for diabetes treatment) pharmacokinetics. It is associated with metformin disposition and response through mediating the transport and excretion of metformin into the urine and bile. A gain-of-function promoter polymorphism (rs12943590 G>A) of SLC47A2 gene is associated with glucose-lowering effects of metformin in type 2 diabetes patients. In addition, compared to the paired adjacent nontumor tissues, the expression of SLC47A2 is significantly decreased in the renal cell carcinoma (RCC) tissue at low tumor node metastasis stage, suggesting that SLC47A2 inhibition may enhance the risk of RCC.

Fig.1 The structural model of human MATE2-K is presented: side view (A) and top view (B). (Nishimura, 2014)

Application of SLC47A2 Membrane Protein in Literature

1. Chowdhury S., et al. MATE2 expression is associated with cancer cell response to metformin. Plos One. 2016, 11(12):e0165214. PubMed ID: 27959931
   
   

   The article reports that the high MATE2 expression may result in resistance to the anti-proliferative effect of metformin and should be considered as a negative predictive biomarker in clinical trials.

2. Yu Q., et al. Histone H3 lysine 4 trimethylation, lysine 27 trimethylation, and lysine 27 acetylation contribute to the transcriptional repression of solute carrier family 47 member 2 in renal cell carcinoma. Drug Metabolism & Disposition the Biological Fate of Chemicals. 2016, 45(1):109-117. PubMed ID: 27821436
   
   

   In the study, results show that the expression of SLC47A2 is significantly decreased in the renal cell carcinoma (RCC) tissue compared to the paired adjacent nontumor tissues at low tumor node metastasis stage. Thus, it is proposed that the inhibition of SLC47A2 may increase the susceptibility of RCC.

3. Choi J.H., et al. A common 5'-UTR variant in MATE2-K is associated with poor response to metformin. Clinical Pharmacology & Therapeutics. 2011, 90(5):674-684. PubMed ID: 21956618
   
   

   The investigation reveals that MATE2-K is involved in the poor response to metformin in patients with diabetes.

4. Toyama K., et al. Heterozygous variants of multidrug and toxin extrusions (MATE1 and MATE2-K) have little influence on the disposition of metformin in diabetic patients. Pharmacogenet Genomics. 2010, 20(2):135-138. PubMed ID: 20016398
   
   

   Results of the study show that heterozygous MATE variants have little effect on the disposition of metformin in diabetic patients.

5. Chung J.Y., et al. Functional characterization of MATE2-K genetic variants and their effects on metformin pharmacokinetics. Pharmacogenetics & Genomics. 2013, 23(7):365-373. PubMed ID: 23652408
   
   

   This metformin pharmacokinetic study determines the association between MATE2-K promoter haplotypes and metformin pharmacokinetics.

SLC47A2 Preparation Options

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Reference

1. Nishimura K, et al. (2014). Identification and functional characterization of novel nonsynonymous variants in the human multidrug and toxin extrusion 2-K. Drug Metabolism & Disposition. 42(9): 1432-1437.

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