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==Structure of native murine cardiac thin filament variant I79N in troponin T at pCa=5.8 in Ca2+-bound fully activated state (upper strand)==
<StructureSection load='9mow' size='340' side='right'caption='[[9mow]], [[Resolution|resolution]] 4.90&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[9mow]] is a 15 chain structure with sequence from [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=9MOW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9MOW 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]] 4.9&#8491;</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=CA:CALCIUM+ION'>CA</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=9mow FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9mow OCA], [https://pdbe.org/9mow PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9mow RCSB], [https://www.ebi.ac.uk/pdbsum/9mow PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9mow ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/TNNT2_HUMAN TNNT2_HUMAN] Defects in TNNT2 are the cause of familial hypertrophic cardiomyopathy type 2 (CMH2) [MIM:[https://omim.org/entry/115195 115195]. Familial hypertrophic cardiomyopathy 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:9482583</ref> <ref>PMID:8205619</ref> <ref>PMID:7898523</ref> <ref>PMID:8989109</ref> <ref>PMID:9060892</ref> [:]<ref>PMID:10525521</ref> <ref>PMID:9140840</ref> <ref>PMID:11034944</ref> <ref>PMID:12707239</ref> <ref>PMID:12974739</ref> <ref>PMID:15563892</ref> <ref>PMID:16199542</ref> <ref>PMID:21846512</ref>   Defects in TNNT2 are the cause of cardiomyopathy dilated type 1D (CMD1D) [MIM:[https://omim.org/entry/601494 601494]. 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:21846512</ref> <ref>PMID:11106718</ref> <ref>PMID:11684629</ref> <ref>PMID:15542288</ref> <ref>PMID:15769782</ref>   Defects in TNNT2 are the cause of familial restrictive cardiomyopathy type 3 (RCM3) [MIM:[https://omim.org/entry/612422 612422]. Restrictive cardiomyopathy is a heart disorder characterized by impaired filling of the ventricles with reduced diastolic volume, in the presence of normal or near normal wall thickness and systolic function.<ref>PMID:16651346</ref> 
== Function ==
[https://www.uniprot.org/uniprot/TNNT2_HUMAN TNNT2_HUMAN] Troponin T is the tropomyosin-binding subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity.
== References ==
<references/>
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</StructureSection>
[[Category: Large Structures]]
[[Category: Mus musculus]]
[[Category: Galkin VE]]
[[Category: Risi CM]]