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HighlightsThiamine transporter 2 (ThTr-2), also known as solute family 19 member 3, is a protein encoded by the SLC19A3 gene. SLC19A3 is a thiamine transporter. This protein regulates high-affinity thiamine absorption through a proton anti-port mechanism. ThTr-2 is an untranslated transmembrane thiamine transporter that lacks the transport activity of folic acid. It is particularly inhibited by chloroquine. Mutation of the gene SLC19A3 leads to thiamine metabolic dysfunction syndrome 2, also known as "bio-triamine reactive basal ganglia disease" (BTBGD).
| Basic Information of SLC19A3 | |
| Protein Name | Thiamine transporter 2 (ThTr2) |
| Gene Name | SLC19A3 |
| Aliases | Solute carrier family 19 member 3 |
| Organism | Homo sapiens (Human) |
| UniProt ID | Q9BZV2 |
| Transmembrane Times | 12 |
| Length (aa) | 496 |
| Sequence | MDCYRTSLSSSWIYPTVILCLFGFFSMMRPSEPFLIPYLSGPDKNLTSAEITNEIFPVWTYSYLVLLLPVFVLTDYVRYKPVIILQGISFIITWLLLLFGQGVKTMQVVEFFYGMVTAAEVAYYAYIYSVVSPEHYQRVSGYCRSVTLAAYTAGSVLAQLLVSLANMSYFYLNVISLASVSVAFLFSLFLPMPKKSMFFHAKPSREIKKSSSVNPVLEETHEGEAPGCEEQKPTSEILSTSGKLNKGQLNSLKPSNVTVDVFVQWFQDLKECYSSKRLFYWSLWWAFATAGFNQVLNYVQILWDYKAPSQDSSIYNGAVEAIATFGGAVAAFAVGYVKVNWDLLGELALVVFSVVNAGSLFLMHYTANIWACYAGYLIFKSSYMLLITIAVFQIAVNLNVERYALVFGINTFIALVIQTIMTVIVVDQRGLNLPVSIQFLVYGSYFAVIAGIFLMRSMYITYSTKSQKDVQSPAPSENPDVSHPEEESNIIMSTKL |
The two transporters of the solute 19 family, THTR1 and THTR2, encoded by the SLC19A2 and SLC19A3 genes, respectively, are responsible for the transport of thiamine on the plasma membrane. THTR2 is widely expressed, expressing the highest THTR2 intestine. Specifically, THTR2 is commonly found in the apical membrane. THTR1 and THTR2 are reverse-transported proton-linked transporters with an affinity for thiamine (km) ~ 2.5μm 27 nm for THTR1 and THTR2. The mutation of SLC10A3 gene leads to bioreactive basal ganglia disease (BBGD).BBGD is a recessive disease in childhood, which if left untreated, will develop into chronic encephalopathy, dystonia, quadriplegia and death. Patients with BBGD have bilateral necrosis in the caudate nucleus and putamen's head. In the early development of the disease, high-dose biotin treatment eliminates pathological symptoms, while delayed treatment leads to residual side effects, mild mental retardation, or dystonia. Administration of thiamine is ineffective in treating this disease. The experiment did not prove that this protein can transport biotin. Mutations in this gene can also cause a Wernicke's-like encephalopathy.
Fig.1 The structure of SLC19A3 Protein.
This study showed the direct binding and activation of SLC19A3 expression by HLC-1α under the hypoxia stress, indicates that hif-1 has an important adaptive regulatory role in the maintenance of thiamine homeostasis.
The new findings suggest that EP2 receptors regulate metastasis through down-regulation of SLC19A3
This deletion is aimed to define the minimal promoter region of SLC19A3 by detecting the smallest promoter deletion reported up to date.
The authors found that a large number of genomic deletions occurred in the regulatory region of SLC19A3 and should be considered in genetic testing.
These results suggest that the progression of neurological diseases leading to death is most likely due to local thiamine deficiency, which is due to a functional mutation that occurs in SLC19A3.1, a gene which codes a thiamine transporter.
To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-SLC19A3 antibody development services.
Creative Biolabs' skillful scientists are glad to leverage our expertise and advanced technologies to help you with the member protein research. If you are interested, please feel free to contact us for more details.
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