6do1: Difference between revisions

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'''Unreleased structure'''


The entry 6do1 is ON HOLD  until Paper Publication
==Structure of nanobody-stabilized angiotensin II type 1 receptor bound to S1I8==
<StructureSection load='6do1' size='340' side='right' caption='[[6do1]], [[Resolution|resolution]] 2.90&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[6do1]] is a 8 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6DO1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6DO1 FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=OLC:(2R)-2,3-DIHYDROXYPROPYL+(9Z)-OCTADEC-9-ENOATE'>OLC</scene></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='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=6do1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6do1 OCA], [http://pdbe.org/6do1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6do1 RCSB], [http://www.ebi.ac.uk/pdbsum/6do1 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6do1 ProSAT]</span></td></tr>
</table>
== 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.
== 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.
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
The angiotensin II (AngII) type 1 receptor (AT1R) is a critical regulator of cardiovascular and renal function and is an important model for studies of G-protein-coupled receptor (GPCR) signaling. By stabilizing the receptor with a single-domain antibody fragment ("nanobody") discovered using a synthetic yeast-displayed library, we determined the crystal structure of active-state human AT1R bound to an AngII analog with partial agonist activity. The nanobody binds to the receptor's intracellular transducer pocket, stabilizing the large conformational changes characteristic of activated GPCRs. The peptide engages the AT1R through an extensive interface spanning from the receptor core to its extracellular face and N terminus, remodeling the ligand-binding cavity. Remarkably, the mechanism used to propagate conformational changes through the receptor diverges from other GPCRs at several key sites, highlighting the diversity of allosteric mechanisms among GPCRs. Our structure provides insight into how AngII and its analogs stimulate full or biased signaling, respectively.


Authors:  
Distinctive Activation Mechanism for Angiotensin Receptor Revealed by a Synthetic Nanobody.,Wingler LM, McMahon C, Staus DP, Lefkowitz RJ, Kruse AC Cell. 2019 Jan 24;176(3):479-490.e12. doi: 10.1016/j.cell.2018.12.006. Epub 2019 , Jan 10. PMID:30639100<ref>PMID:30639100</ref>


Description:  
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
[[Category: Unreleased Structures]]
</div>
<div class="pdbe-citations 6do1" style="background-color:#fffaf0;"></div>
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Kruse, A C]]
[[Category: Lefkowitz, R J]]
[[Category: McMahon, C]]
[[Category: Staus, D P]]
[[Category: Wingler, L M]]
[[Category: Gpcr]]
[[Category: Membrane protein]]
[[Category: Nanobody]]
[[Category: Synthetic antibody]]

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