5lm4
From Proteopedia
(Difference between revisions)
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| - | '''Unreleased structure''' | ||
| - | + | ==Structure of the thermostalilized EAAT1 cryst-II mutant in complex with L-ASP and the allosteric inhibitor UCPH101== | |
| - | + | <StructureSection load='5lm4' size='340' side='right' caption='[[5lm4]], [[Resolution|resolution]] 3.10Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[5lm4]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5LM4 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5LM4 FirstGlance]. <br> | |
| - | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=6Z6:2-AMINO-5,6,7,8-TETRAHYDRO-4-(4-METHOXYPHENYL)-7-(NAPHTHALEN-1-YL)-5-OXO-4H-CHROMENE-3-CARBONITRILE'>6Z6</scene>, <scene name='pdbligand=ASP:ASPARTIC+ACID'>ASP</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr> | |
| - | [[Category: | + | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5llm|5llm]]</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=5lm4 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5lm4 OCA], [http://pdbe.org/5lm4 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5lm4 RCSB], [http://www.ebi.ac.uk/pdbsum/5lm4 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5lm4 ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
| + | [[http://www.uniprot.org/uniprot/EAA1_HUMAN EAA1_HUMAN]] Alternating hemiplegia of childhood;Episodic ataxia type 6. The disease is caused by mutations affecting the gene represented in this entry. | ||
| + | == Function == | ||
| + | [[http://www.uniprot.org/uniprot/EAA1_HUMAN EAA1_HUMAN]] Transports L-glutamate and also L- and D-aspartate. Essential for terminating the postsynaptic action of glutamate by rapidly removing released glutamate from the synaptic cleft. Acts as a symport by cotransporting sodium. | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
| + | [[Category: Assal, R]] | ||
| + | [[Category: Canul-Tec, J]] | ||
| + | [[Category: Legrand, P]] | ||
| + | [[Category: Reyes, N]] | ||
| + | [[Category: Excitatory amino acid transporter 1]] | ||
| + | [[Category: Human glutamate transporter]] | ||
| + | [[Category: Slc1a3]] | ||
| + | [[Category: Transport protein]] | ||
| + | [[Category: Ucph101]] | ||
Revision as of 12:59, 19 April 2017
Structure of the thermostalilized EAAT1 cryst-II mutant in complex with L-ASP and the allosteric inhibitor UCPH101
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