1zll
From Proteopedia
(Difference between revisions)
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<StructureSection load='1zll' size='340' side='right'caption='[[1zll]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | <StructureSection load='1zll' size='340' side='right'caption='[[1zll]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
- | <table><tr><td colspan='2'>[[1zll]] is a 5 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[1zll]] is a 5 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1ZLL OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1ZLL FirstGlance]. <br> |
- | </td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PLN ([ | + | </td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">PLN ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr> |
- | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1zll FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1zll OCA], [https://pdbe.org/1zll PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1zll RCSB], [https://www.ebi.ac.uk/pdbsum/1zll PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1zll ProSAT]</span></td></tr> |
</table> | </table> | ||
== Disease == | == Disease == | ||
- | [[ | + | [[https://www.uniprot.org/uniprot/PPLA_HUMAN PPLA_HUMAN]] Defects in PLN are the cause of cardiomyopathy dilated type 1P (CMD1P) [MIM:[https://omim.org/entry/609909 609909]]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.<ref>PMID:12610310</ref> <ref>PMID:16432188</ref> Defects in PLN are the cause of familial hypertrophic cardiomyopathy type 18 (CMH18) [MIM:[https://omim.org/entry/613874 613874]]. CMH18 is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.<ref>PMID:12705874</ref> |
== Function == | == Function == | ||
- | [[ | + | [[https://www.uniprot.org/uniprot/PPLA_HUMAN PPLA_HUMAN]] Phospholamban has been postulated to regulate the activity of the calcium pump of cardiac sarcoplasmic reticulum. |
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == |
Revision as of 07:17, 2 March 2022
NMR Structure of Unphosphorylated Human Phospholamban Pentamer
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