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| <StructureSection load='4pyp' size='340' side='right'caption='[[4pyp]], [[Resolution|resolution]] 3.17Å' scene=''> | | <StructureSection load='4pyp' size='340' side='right'caption='[[4pyp]], [[Resolution|resolution]] 3.17Å' scene=''> |
| == Structural highlights == | | == Structural highlights == |
- | <table><tr><td colspan='2'>[[4pyp]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4PYP OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4PYP FirstGlance]. <br> | + | <table><tr><td colspan='2'>[[4pyp]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4PYP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4PYP FirstGlance]. <br> |
- | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BNG:B-NONYLGLUCOSIDE'>BNG</scene></td></tr> | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=BNG:B-NONYLGLUCOSIDE'>BNG</scene></td></tr> |
- | <tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">SLC2A1, GLUT1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
| + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4pyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pyp OCA], [https://pdbe.org/4pyp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4pyp RCSB], [https://www.ebi.ac.uk/pdbsum/4pyp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4pyp ProSAT]</span></td></tr> |
- | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4pyp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pyp OCA], [http://pdbe.org/4pyp PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4pyp RCSB], [http://www.ebi.ac.uk/pdbsum/4pyp PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4pyp ProSAT]</span></td></tr> | + | |
| </table> | | </table> |
| == Disease == | | == Disease == |
- | [[http://www.uniprot.org/uniprot/GTR1_HUMAN GTR1_HUMAN]] Hereditary cryohydrocytosis with reduced stomatin;Paroxysmal exertion-induced dyskinesia;Encephalopathy due to GLUT1 deficiency;Paroxysmal dystonic choreathetosis with episodic ataxia and spasticity;Childhood absence epilepsy;Epilepsy with myoclonic-astatic seizures. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. | + | [https://www.uniprot.org/uniprot/GTR1_HUMAN GTR1_HUMAN] Hereditary cryohydrocytosis with reduced stomatin;Paroxysmal exertion-induced dyskinesia;Encephalopathy due to GLUT1 deficiency;Paroxysmal dystonic choreathetosis with episodic ataxia and spasticity;Childhood absence epilepsy;Epilepsy with myoclonic-astatic seizures. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. |
| == Function == | | == Function == |
- | [[http://www.uniprot.org/uniprot/GTR1_HUMAN GTR1_HUMAN]] Facilitative glucose transporter. This isoform may be responsible for constitutive or basal glucose uptake. Has a very broad substrate specificity; can transport a wide range of aldoses including both pentoses and hexoses. | + | [https://www.uniprot.org/uniprot/GTR1_HUMAN GTR1_HUMAN] Facilitative glucose transporter. This isoform may be responsible for constitutive or basal glucose uptake. Has a very broad substrate specificity; can transport a wide range of aldoses including both pentoses and hexoses. |
| <div style="background-color:#fffaf0;"> | | <div style="background-color:#fffaf0;"> |
| == Publication Abstract from PubMed == | | == Publication Abstract from PubMed == |
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| </div> | | </div> |
| <div class="pdbe-citations 4pyp" style="background-color:#fffaf0;"></div> | | <div class="pdbe-citations 4pyp" style="background-color:#fffaf0;"></div> |
| + | |
| + | ==See Also== |
| + | *[[ABC transporter 3D structures|ABC transporter 3D structures]] |
| == References == | | == References == |
| <references/> | | <references/> |
| __TOC__ | | __TOC__ |
| </StructureSection> | | </StructureSection> |
- | [[Category: Human]] | + | [[Category: Homo sapiens]] |
| [[Category: Large Structures]] | | [[Category: Large Structures]] |
- | [[Category: Deng, D]] | + | [[Category: Deng D]] |
- | [[Category: Hu, M X]] | + | [[Category: Hu MX]] |
- | [[Category: Sun, P C]] | + | [[Category: Sun PC]] |
- | [[Category: Wu, J P]] | + | [[Category: Wu JP]] |
- | [[Category: Xu, C]] | + | [[Category: Xu C]] |
- | [[Category: Yan, C Y]] | + | [[Category: Yan CY]] |
- | [[Category: Yan, N]] | + | [[Category: Yan N]] |
- | [[Category: Glycosylation]]
| + | |
- | [[Category: Helix]]
| + | |
- | [[Category: Membrane transporter]]
| + | |
- | [[Category: Transport protein]]
| + | |
| Structural highlights
Disease
GTR1_HUMAN Hereditary cryohydrocytosis with reduced stomatin;Paroxysmal exertion-induced dyskinesia;Encephalopathy due to GLUT1 deficiency;Paroxysmal dystonic choreathetosis with episodic ataxia and spasticity;Childhood absence epilepsy;Epilepsy with myoclonic-astatic seizures. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
Function
GTR1_HUMAN Facilitative glucose transporter. This isoform may be responsible for constitutive or basal glucose uptake. Has a very broad substrate specificity; can transport a wide range of aldoses including both pentoses and hexoses.
Publication Abstract from PubMed
The glucose transporter GLUT1 catalyses facilitative diffusion of glucose into erythrocytes and is responsible for glucose supply to the brain and other organs. Dysfunctional mutations may lead to GLUT1 deficiency syndrome, whereas overexpression of GLUT1 is a prognostic indicator for cancer. Despite decades of investigation, the structure of GLUT1 remains unknown. Here we report the crystal structure of human GLUT1 at 3.2 A resolution. The full-length protein, which has a canonical major facilitator superfamily fold, is captured in an inward-open conformation. This structure allows accurate mapping and potential mechanistic interpretation of disease-associated mutations in GLUT1. Structure-based analysis of these mutations provides an insight into the alternating access mechanism of GLUT1 and other members of the sugar porter subfamily. Structural comparison of the uniporter GLUT1 with its bacterial homologue XylE, a proton-coupled xylose symporter, allows examination of the transport mechanisms of both passive facilitators and active transporters.
Crystal structure of the human glucose transporter GLUT1.,Deng D, Xu C, Sun P, Wu J, Yan C, Hu M, Yan N Nature. 2014 Jun 5;510(7503):121-5. doi: 10.1038/nature13306. Epub 2014 May 18. PMID:24847886[1]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
See Also
References
- ↑ Deng D, Xu C, Sun P, Wu J, Yan C, Hu M, Yan N. Crystal structure of the human glucose transporter GLUT1. Nature. 2014 Jun 5;510(7503):121-5. doi: 10.1038/nature13306. Epub 2014 May 18. PMID:24847886 doi:http://dx.doi.org/10.1038/nature13306
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