8sgc: Difference between revisions
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New page: '''Unreleased structure''' The entry 8sgc is ON HOLD Authors: Wang, S., Sass, M., Willardson, B.M., Shen, P.S. Description: CCT G beta 5 complex closed state 2 [[Category: Unreleased S... |
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==CCT G beta 5 complex closed state 2== | |||
<StructureSection load='8sgc' size='340' side='right'caption='[[8sgc]], [[Resolution|resolution]] 2.90Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[8sgc]] is a 18 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=8SGC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8SGC 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]] 2.9Å</td></tr> | |||
[[Category: | <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> | ||
[[Category: Sass | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8sgc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8sgc OCA], [https://pdbe.org/8sgc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8sgc RCSB], [https://www.ebi.ac.uk/pdbsum/8sgc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8sgc ProSAT]</span></td></tr> | ||
[[Category: Shen | </table> | ||
[[Category: | == Disease == | ||
[[Category: | [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> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Sass M]] | |||
[[Category: Shen PS]] | |||
[[Category: Wang S]] | |||
[[Category: Willardson BM]] | |||
Latest revision as of 10:08, 25 October 2023
CCT G beta 5 complex closed state 2CCT G beta 5 complex closed state 2
Structural highlights
DiseaseGNB5_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. FunctionGNB5_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][1] References
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