8she
From Proteopedia
(Difference between revisions)
(New page: '''Unreleased structure''' The entry 8she is ON HOLD Authors: Wang, S., Sass, M., Willardson, B.M., Shen, P.S. Description: CCT-G beta 5 complex closed state 8 [[Category: Unreleased S...) |
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- | '''Unreleased structure''' | ||
- | The entry | + | ==CCT-G beta 5 complex closed state 8== |
+ | <StructureSection load='8she' size='340' side='right'caption='[[8she]], [[Resolution|resolution]] 2.80Å' scene=''> | ||
+ | == Structural highlights == | ||
+ | <table><tr><td colspan='2'>[[8she]] is a 17 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=8SHE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8SHE 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]] 2.8Å</td></tr> | ||
+ | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=AF3:ALUMINUM+FLUORIDE'>AF3</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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=8she FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8she OCA], [https://pdbe.org/8she PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8she RCSB], [https://www.ebi.ac.uk/pdbsum/8she PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8she ProSAT]</span></td></tr> | ||
+ | </table> | ||
+ | == Disease == | ||
+ | [https://www.uniprot.org/uniprot/GNB5_HUMAN GNB5_HUMAN] GNB5-related intellectual disability-cardiac arrhythmia syndrome. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. | ||
+ | == Function == | ||
+ | [https://www.uniprot.org/uniprot/GNB5_HUMAN GNB5_HUMAN] Enhances GTPase-activating protein (GAP) activity of regulator of G protein signaling (RGS) proteins, such as RGS7 and RGS9, hence involved in the termination of the signaling initiated by the G protein coupled receptors (GPCRs) by accelerating the GTP hydrolysis on the G-alpha subunits, thereby promoting their inactivation (PubMed:27677260). Increases RGS7 GTPase-activating protein (GAP) activity, thereby regulating mood and cognition (By similarity). Increases RGS9 GTPase-activating protein (GAP) activity, hence contributes to the deactivation of G protein signaling initiated by D(2) dopamine receptors (PubMed:27677260). May play an important role in neuronal signaling, including in the parasympathetic, but not sympathetic, control of heart rate (By similarity).[UniProtKB:A1L271][UniProtKB:P62881]<ref>PMID:27677260</ref> | ||
- | + | ==See Also== | |
- | + | *[[Transducin 3D structures|Transducin 3D structures]] | |
- | + | == References == | |
- | [[Category: | + | <references/> |
- | [[Category: | + | __TOC__ |
- | [[Category: Sass | + | </StructureSection> |
- | [[Category: Shen | + | [[Category: Homo sapiens]] |
- | [[Category: Willardson | + | [[Category: Large Structures]] |
+ | [[Category: Sass M]] | ||
+ | [[Category: Shen PS]] | ||
+ | [[Category: Wang S]] | ||
+ | [[Category: Willardson BM]] |
Current revision
CCT-G beta 5 complex closed state 8
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