8she

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
-
'''Unreleased structure'''
 
-
The entry 8she is ON HOLD until Paper Publication
+
==CCT-G beta 5 complex closed state 8==
-
 
+
<StructureSection load='8she' size='340' side='right'caption='[[8she]], [[Resolution|resolution]] 2.80&Aring;' scene=''>
-
Authors: Wang, S., Sass, M., Willardson, B.M., Shen, P.S.
+
== 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>
-
Description: CCT-G beta 5 complex closed state 8
+
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 2.8&#8491;</td></tr>
-
[[Category: Unreleased Structures]]
+
<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, M]]
+
<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>
-
[[Category: Shen, P.S]]
+
</table>
-
[[Category: Willardson, B.M]]
+
== Disease ==
-
[[Category: Wang, S]]
+
[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]]

Revision as of 07:08, 25 October 2023

CCT-G beta 5 complex closed state 8

PDB ID 8she

Drag the structure with the mouse to rotate

Proteopedia Page Contributors and Editors (what is this?)

OCA

Personal tools