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8uxf
From Proteopedia
(Difference between revisions)
(New page: '''Unreleased structure''' The entry 8uxf is ON HOLD Authors: Miotto, M.C., Marks, A.R. Description: Structure of PKA phosphorylated human RyR2-R420W in the primed state [[Category: Un...) |
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| - | '''Unreleased structure''' | ||
| - | + | ==Structure of PKA phosphorylated human RyR2-R420W in the primed state== | |
| - | + | <StructureSection load='8uxf' size='340' side='right'caption='[[8uxf]], [[Resolution|resolution]] 3.13Å' scene=''> | |
| - | + | == Structural highlights == | |
| - | + | <table><tr><td colspan='2'>[[8uxf]] is a 8 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=8UXF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8UXF 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]] 3.13Å</td></tr> | |
| - | [[Category: | + | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ATP:ADENOSINE-5-TRIPHOSPHATE'>ATP</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr> |
| - | [[Category: | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8uxf FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8uxf OCA], [https://pdbe.org/8uxf PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8uxf RCSB], [https://www.ebi.ac.uk/pdbsum/8uxf PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8uxf ProSAT]</span></td></tr> |
| - | [[Category: Marks | + | </table> |
| + | == Disease == | ||
| + | [https://www.uniprot.org/uniprot/RYR2_HUMAN RYR2_HUMAN] Familial isolated arrhythmogenic ventricular dysplasia, right dominant form;Catecholaminergic polymorphic ventricular tachycardia;Familial isolated arrhythmogenic ventricular dysplasia, biventricular form;Familial isolated arrhythmogenic ventricular dysplasia, left dominant form. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. | ||
| + | == Function == | ||
| + | [https://www.uniprot.org/uniprot/RYR2_HUMAN RYR2_HUMAN] Calcium channel that mediates the release of Ca(2+) from the sarcoplasmic reticulum into the cytoplasm and thereby plays a key role in triggering cardiac muscle contraction. Aberrant channel activation can lead to cardiac arrhythmia. In cardiac myocytes, calcium release is triggered by increased Ca(2+) levels due to activation of the L-type calcium channel CACNA1C. The calcium channel activity is modulated by formation of heterotetramers with RYR3. Required for cellular calcium ion homeostasis. Required for embryonic heart development.<ref>PMID:10830164</ref> <ref>PMID:20056922</ref> | ||
| + | == References == | ||
| + | <references/> | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
| + | [[Category: Homo sapiens]] | ||
| + | [[Category: Large Structures]] | ||
| + | [[Category: Marks AR]] | ||
| + | [[Category: Miotto MC]] | ||
Current revision
Structure of PKA phosphorylated human RyR2-R420W in the primed state
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