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| | <StructureSection load='6os1' size='340' side='right'caption='[[6os1]], [[Resolution|resolution]] 2.79Å' scene=''> | | <StructureSection load='6os1' size='340' side='right'caption='[[6os1]], [[Resolution|resolution]] 2.79Å' scene=''> |
| | == Structural highlights == | | == Structural highlights == |
| - | <table><tr><td colspan='2'>[[6os1]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/"bacillus_coli"_migula_1895 "bacillus coli" migula 1895] and [http://en.wikipedia.org/wiki/Synthetic_construct_sequences Synthetic construct sequences]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6OS1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6OS1 FirstGlance]. <br> | + | <table><tr><td colspan='2'>[[6os1]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Escherichia_coli Escherichia coli], [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6OS1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6OS1 FirstGlance]. <br> |
| - | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CLR:CHOLESTEROL'>CLR</scene>, <scene name='pdbligand=OLC:(2R)-2,3-DIHYDROXYPROPYL+(9Z)-OCTADEC-9-ENOATE'>OLC</scene></td></tr> | + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.794Å</td></tr> |
| - | <tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SAR:SARCOSINE'>SAR</scene></td></tr> | + | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CLR:CHOLESTEROL'>CLR</scene>, <scene name='pdbligand=OLC:(2R)-2,3-DIHYDROXYPROPYL+(9Z)-OCTADEC-9-ENOATE'>OLC</scene>, <scene name='pdbligand=SAR:SARCOSINE'>SAR</scene></td></tr> |
| - | <tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">AGTR1, AGTR1A, AGTR1B, AT2R1, AT2R1B ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=562 "Bacillus coli" Migula 1895])</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=6os1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6os1 OCA], [https://pdbe.org/6os1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6os1 RCSB], [https://www.ebi.ac.uk/pdbsum/6os1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6os1 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=6os1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6os1 OCA], [http://pdbe.org/6os1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6os1 RCSB], [http://www.ebi.ac.uk/pdbsum/6os1 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6os1 ProSAT]</span></td></tr> | + | |
| | </table> | | </table> |
| | == Disease == | | == Disease == |
| - | [[http://www.uniprot.org/uniprot/AGTR1_HUMAN AGTR1_HUMAN]] NON RARE IN EUROPE: Essential hypertension;Renal tubular dysgenesis of genetic origin. The disease is caused by mutations affecting the gene represented in this entry. | + | [https://www.uniprot.org/uniprot/AGTR1_HUMAN AGTR1_HUMAN] NON RARE IN EUROPE: Essential hypertension;Renal tubular dysgenesis of genetic origin. The disease is caused by mutations affecting the gene represented in this entry. |
| | == Function == | | == Function == |
| - | [[http://www.uniprot.org/uniprot/AGTR1_HUMAN AGTR1_HUMAN]] Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system. | + | [https://www.uniprot.org/uniprot/C562_ECOLX C562_ECOLX] Electron-transport protein of unknown function.[https://www.uniprot.org/uniprot/AGTR1_HUMAN AGTR1_HUMAN] Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system. |
| | <div style="background-color:#fffaf0;"> | | <div style="background-color:#fffaf0;"> |
| | == Publication Abstract from PubMed == | | == Publication Abstract from PubMed == |
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| | __TOC__ | | __TOC__ |
| | </StructureSection> | | </StructureSection> |
| - | [[Category: Bacillus coli migula 1895]] | + | [[Category: Escherichia coli]] |
| | + | [[Category: Homo sapiens]] |
| | [[Category: Large Structures]] | | [[Category: Large Structures]] |
| - | [[Category: Synthetic construct sequences]] | + | [[Category: Synthetic construct]] |
| - | [[Category: Kleinhenz, A L.W]] | + | [[Category: Kleinhenz ALW]] |
| - | [[Category: Kruse, A C]] | + | [[Category: Kruse AC]] |
| - | [[Category: Lefkowitz, R J]] | + | [[Category: Lefkowitz RJ]] |
| - | [[Category: McMahon, C]] | + | [[Category: McMahon C]] |
| - | [[Category: Skiba, M A]] | + | [[Category: Skiba MA]] |
| - | [[Category: Staus, D P]] | + | [[Category: Staus DP]] |
| - | [[Category: Wingler, L M]] | + | [[Category: Wingler LM]] |
| - | [[Category: Gpcr]]
| + | |
| - | [[Category: Membrane protein]]
| + | |
| Structural highlights
Disease
AGTR1_HUMAN NON RARE IN EUROPE: Essential hypertension;Renal tubular dysgenesis of genetic origin. The disease is caused by mutations affecting the gene represented in this entry.
Function
C562_ECOLX Electron-transport protein of unknown function.AGTR1_HUMAN Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system.
Publication Abstract from PubMed
Biased agonists of G protein-coupled receptors (GPCRs) preferentially activate a subset of downstream signaling pathways. In this work, we present crystal structures of angiotensin II type 1 receptor (AT1R) (2.7 to 2.9 angstroms) bound to three ligands with divergent bias profiles: the balanced endogenous agonist angiotensin II (AngII) and two strongly beta-arrestin-biased analogs. Compared with other ligands, AngII promotes more-substantial rearrangements not only at the bottom of the ligand-binding pocket but also in a key polar network in the receptor core, which forms a sodium-binding site in most GPCRs. Divergences from the family consensus in this region, which appears to act as a biased signaling switch, may predispose the AT1R and certain other GPCRs (such as chemokine receptors) to adopt conformations that are capable of activating beta-arrestin but not heterotrimeric Gq protein signaling.
Angiotensin and biased analogs induce structurally distinct active conformations within a GPCR.,Wingler LM, Skiba MA, McMahon C, Staus DP, Kleinhenz ALW, Suomivuori CM, Latorraca NR, Dror RO, Lefkowitz RJ, Kruse AC Science. 2020 Feb 21;367(6480):888-892. doi: 10.1126/science.aay9813. PMID:32079768[1]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
References
- ↑ Wingler LM, Skiba MA, McMahon C, Staus DP, Kleinhenz ALW, Suomivuori CM, Latorraca NR, Dror RO, Lefkowitz RJ, Kruse AC. Angiotensin and biased analogs induce structurally distinct active conformations within a GPCR. Science. 2020 Feb 21;367(6480):888-892. doi: 10.1126/science.aay9813. PMID:32079768 doi:http://dx.doi.org/10.1126/science.aay9813
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