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HighlightsIntroduction 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.
| Basic Information of SLC52A1 | |
| Protein Name | Solute carrier family 52, riboflavin transporter, member 1 |
| Gene Name | SLC52A1 |
| Aliases | PAR2, RFT1, RBFVD, RFVT1, hRFT1, GPCR42, GPR172B |
| Organism | Homo sapiens (Human) |
| UniProt ID | Q86UW2 |
| Transmembrane Times | 11 |
| Length (aa) | 448 |
| Sequence | MAAPTLGRLVLTHLLVALFGMGSWAAVNGIWVELPVVVKDLPEGWSLPSYLSVVVALGNLGLLVVTLWRQLAPGKGEQVPIQVVQVLSVVGTALLAPLWHHVAPVAGQLHSVAFLTLALVLAMACCTSNVTFLPFLSHLPPPFLRSFFLGQGLSALLPCVLALVQGVGRLECPPAPTNGTSGPPLDFPERFPASTFFWALTALLVTSAAAFRGLLLLLPSLPSVTTGGSGPELQLGSPGAEEEEKEEEEALPLQEPPSQAAGTIPGPDPEAHQLFSAHGAFLLGLMAFTSAVTNGVLPSVQSFSCLPYGRLAYHLAVVLGSAANPLACFLAMGVLCRSLAGLVGLSLLGMLFGAYLMALAILSPCPPLVGTTAGVVLVVLSWVLCLCVFSYVKVAASSLLHGGGRPALLAAGVAIQVGSLLGAGAMFPPTSIYHVFQSRKDCVDPCGP |
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
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.
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.
The study reports a heterozygous intronic variation (c.1134+11G>A) in the SLC52A1 gene is associated with multiple acyl-CoA dehydrogenation deficiencies (MADD).
In this study, authors assess the contribution of each human RFVT to riboflavin, FMN and FAD uptake and efflux using in vitro studies.
The study reveals that three cysteine residues of SLC52A1 play an important role in the surface expression and PERV-A infection.
SLC52A1 Preparation Options
Based on the versatile Magic™ membrane protein production platform, Creative Biolabs can help you to obtain the best soluble and functional target protein to make your project a success. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-SLC52A1 antibody development services.
As a forward-looking research institute as well as a leading custom service provider in the field of membrane protein, Creative Biolabs has won good reputation among our worldwide customers for successfully accomplishing numerous challenging projects including generation of many functional membrane proteins. Please feel free to contact us for more information.
Reference
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