SLC52A1 Membrane Protein Introduction

Introduction of SLC52A1

SLC52A1 encoded by SLC52A1 gene, also known as PAR2, is a 448-amino acid, 11-transmembrane (TM) domain protein. It belongs to riboflavin (vitamin B2) transporter family that is involved in riboflavin transport. Now three novel riboflavin transporters have been identified and named as RFVT1/SLC52A1, RFVT2/SLC52A2 and RFVT3/SLC52A3. SLC52A1 is highly expressed in the placenta and small intestine. SLC52A2 is expressed ubiquitously, especially higher in the brain and salivary gland. SLC52A3 is predominantly expressed in the testis and small intestine.

Function of SLC52A1 Membrane Protein

SLC52A1 (RFVT1) is a riboflavin transporter that is involved in the translocation across the plasma membrane of riboflavin. It is Na⁺-independent but not pH-sensitive transporter that mediates the riboflavin uptake independent of extracellular Na⁺ and Cl^- and H⁺ concentration. Riboflavin, also known as vitamin B2, is essential for normal cellular functions. The riboflavin deficiency can lead to multiple acyl-CoA dehydrogenase deficiencies (MADD), or glutaric aciduria type II which is an autosomal recessive disorder mainly influencing amino acid and fatty acid metabolism. Mutations in SLC52A1 have been revealed to be associated with riboflavin deficiency and MADD. The pregnancy with SLC52A1 deficiency and nutritional riboflavin deficiency can result in the transient riboflavin responsive disease seen in her newborn infant. In addition, a recent study reveals that RFVT1 may exert a role in colorectal cancer (CRC). Both protein and mRNA levels of RFVT1 are decreased in tumor tissues of patients with CRC compared to normal mucosa.

Fig.1 Intestinal absorption and tissue distribution of riboflavin mediated by RFVT. (Yonezawa, 2013)

Application of SLC52A1 Membrane Protein in Literature

1. Ho G., et al. Maternal riboflavin deficiency, resulting in transient neonatal-onset glutaric aciduria Type 2, is caused by a microdeletion in the riboflavin transporter gene GPR172B. Human Mutation. 2011, 32(1): E1976-E1984. PubMed ID: 21089064
   
   

   The article indicates that a microdeletion in the riboflavin transporter gene GPR172B causes maternal riboflavin deficiency and then results in transient riboflavin-responsive disease in her newborn infant.

2. Tutino V., et al. The expression of riboflavin transporters in human colorectal cancer. Anticancer Research. 2018, 38(5): 2659-2667. PubMed ID: 29715086
   
   

   The data in this study show that both protein and mRNA levels of RFVT1 are decreased in tumor tissues of patients with CRC compared to normal mucosa.

3. Mosegaard S., et al. An intronic variation in SLC52A1 causes exon skipping and transient riboflavin-responsive multiple acyl-CoA dehydrogenation deficiency. Molecular Genetics & Metabolism. 2017, 122(4): 182-188. PubMed ID: 29122468
   
   

   The study reports a heterozygous intronic variation (c.1134+11G>A) in the SLC52A1 gene is associated with multiple acyl-CoA dehydrogenation deficiencies (MADD).

4. Jin C., et al. Riboflavin transporters RFVT/SLC52A mediate translocation of riboflavin, rather than FMN or FAD, across plasma membrane. Biological & Pharmaceutical Bulletin. 2017, 40(11): 1990-1995. PubMed ID: 29093349
   
   

   In this study, authors assess the contribution of each human RFVT to riboflavin, FMN and FAD uptake and efflux using in vitro studies.

5. Colon-Moran W., et al. Three cysteine residues of SLC52A1, a receptor for the porcine endogenous retrovirus-A (PERV-A), play a critical role in cell surface expression and infectivity. Virology. 2017, 507: 140-150. PubMed ID: 28437635
   
   

   The study reveals that three cysteine residues of SLC52A1 play an important role in the surface expression and PERV-A infection.

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Reference

1. Yonezawa A and Inui K. (2013). Novel riboflavin transporter family RFVT/SLC52: identification, nomenclature, functional characterization and genetic diseases of RFVT/SLC52. Molecular Aspects of Medicine. 34(2-3), 693-701.

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