View source for 27tm


==GRM1-Acc State Conformation 2==
<StructureSection load='27tm' size='340' side='right'caption='[[27tm]], [[Resolution|resolution]] 3.20&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[27tm]] is a 2 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=27TM OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=27TM FirstGlance]. <br>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.2&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=A1EX5:~{N}-[4-(trifluoromethyl)-1,3-oxazol-2-yl]-9~{H}-xanthene-9-carboxamide'>A1EX5</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=CLR:CHOLESTEROL'>CLR</scene>, <scene name='pdbligand=GGL:GAMMA-L-GLUTAMIC+ACID'>GGL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></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=27tm FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=27tm OCA], [https://pdbe.org/27tm PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=27tm RCSB], [https://www.ebi.ac.uk/pdbsum/27tm PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=27tm ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/GRM1_HUMAN GRM1_HUMAN] Autosomal recessive congenital cerebellar ataxia due to MGLUR1 deficiency. The disease is caused by mutations affecting the gene represented in this entry.<ref>PMID:22901947</ref> 
== Function ==
[https://www.uniprot.org/uniprot/GRM1_HUMAN GRM1_HUMAN] G-protein coupled receptor for glutamate. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors. Signaling activates a phosphatidylinositol-calcium second messenger system. May participate in the central action of glutamate in the CNS, such as long-term potentiation in the hippocampus and long-term depression in the cerebellum.<ref>PMID:7476890</ref> 
== References ==
<references/>
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</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Lu Y]]
[[Category: Shen YQ]]
[[Category: Wen TL]]
[[Category: Yang X]]