1j1d: Difference between revisions

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 ==Crystal structure of the 46kDa domain of human cardiac troponin in the Ca2+ saturated form==
-<StructureSection load='1j1d' size='340' side='right' caption='[[1j1d]], [[Resolution|resolution]] 2.61&Aring;' scene=''>
+<StructureSection load='1j1d' size='340' side='right'caption='[[1j1d]], [[Resolution|resolution]] 2.61&Aring;' scene=''>
 == Structural highlights ==
-<table><tr><td colspan='2'>[[1j1d]] is a 6 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1J1D OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1J1D FirstGlance]. <br>
+<table><tr><td colspan='2'>[[1j1d]] is a 6 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=1J1D OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1J1D FirstGlance]. <br>
-</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene></td></tr>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.61&#8491;</td></tr>
-<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1j1e|1j1e]]</td></tr>
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene></td></tr>
-<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1j1d FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1j1d OCA], [http://pdbe.org/1j1d PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1j1d RCSB], [http://www.ebi.ac.uk/pdbsum/1j1d PDBsum]</span></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=1j1d FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1j1d OCA], [https://pdbe.org/1j1d PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1j1d RCSB], [https://www.ebi.ac.uk/pdbsum/1j1d PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1j1d ProSAT]</span></td></tr>
 </table>
 == Disease ==
-[[http://www.uniprot.org/uniprot/TNNC1_HUMAN TNNC1_HUMAN]] Defects in TNNC1 are the cause of cardiomyopathy dilated type 1Z (CMD1Z) [MIM:[http://omim.org/entry/611879 611879]]. 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:15542288</ref>   Defects in TNNC1 are the cause of familial hypertrophic cardiomyopathy type 13 (CMH13) [MIM:[http://omim.org/entry/613243 613243]]. 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:11385718</ref> <ref>PMID:16302972</ref> <ref>PMID:18572189</ref> <ref>PMID:19439414</ref>  [[http://www.uniprot.org/uniprot/TNNI3_HUMAN TNNI3_HUMAN]] Defects in TNNI3 are the cause of familial hypertrophic cardiomyopathy type 7 (CMH7) [MIM:[http://omim.org/entry/613690 613690]]. 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:9241277</ref> <ref>PMID:11815426</ref> <ref>PMID:12707239</ref> <ref>PMID:12974739</ref> <ref>PMID:16199542</ref>   Defects in TNNI3 are the cause of familial restrictive cardiomyopathy type 1 (RCM1) [MIM:[http://omim.org/entry/115210 115210]]. RCM1 is a heart muscle 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:12531876</ref>   Defects in TNNI3 are the cause of cardiomyopathy dilated type 2A (CMD2A) [MIM:[http://omim.org/entry/611880 611880]]. 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:15070570</ref>   Defects in TNNI3 are the cause of cardiomyopathy dilated type 1FF (CMD1FF) [MIM:[http://omim.org/entry/613286 613286]]. 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. [[http://www.uniprot.org/uniprot/TNNT2_HUMAN TNNT2_HUMAN]] Defects in TNNT2 are the cause of familial hypertrophic cardiomyopathy type 2 (CMH2) [MIM:[http://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:[http://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:[http://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>
+[https://www.uniprot.org/uniprot/TNNC1_HUMAN TNNC1_HUMAN] Defects in TNNC1 are the cause of cardiomyopathy dilated type 1Z (CMD1Z) [MIM:[https://omim.org/entry/611879 611879]. 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:15542288</ref>   Defects in TNNC1 are the cause of familial hypertrophic cardiomyopathy type 13 (CMH13) [MIM:[https://omim.org/entry/613243 613243]. 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:11385718</ref> <ref>PMID:16302972</ref> <ref>PMID:18572189</ref> <ref>PMID:19439414</ref>
 == Function ==
-[[http://www.uniprot.org/uniprot/TNNC1_HUMAN TNNC1_HUMAN]] Troponin is the central regulatory protein of striated muscle contraction. Tn consists of three components: Tn-I which is the inhibitor of actomyosin ATPase, Tn-T which contains the binding site for tropomyosin and Tn-C. The binding of calcium to Tn-C abolishes the inhibitory action of Tn on actin filaments. [[http://www.uniprot.org/uniprot/TNNI3_HUMAN TNNI3_HUMAN]] Troponin I is the inhibitory subunit of troponin, the thin filament regulatory complex which confers calcium-sensitivity to striated muscle actomyosin ATPase activity. [[http://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.
+[https://www.uniprot.org/uniprot/TNNC1_HUMAN TNNC1_HUMAN] Troponin is the central regulatory protein of striated muscle contraction. Tn consists of three components: Tn-I which is the inhibitor of actomyosin ATPase, Tn-T which contains the binding site for tropomyosin and Tn-C. The binding of calcium to Tn-C abolishes the inhibitory action of Tn on actin filaments.
 == Evolutionary Conservation ==
 [[Image:Consurf_key_small.gif|200px|right]]
 Check<jmol>
    <jmolCheckbox>
-     <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/j1/1j1d_consurf.spt"</scriptWhenChecked>
+     <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/j1/1j1d_consurf.spt"</scriptWhenChecked>
      <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
      <text>to colour the structure by Evolutionary Conservation</text>
@@ Line 32: / Line 33: @@
 ==See Also==
-*[[Troponin|Troponin]]
+*[[Troponin 3D structures|Troponin 3D structures]]
 == References ==
 <references/>
 __TOC__
 </StructureSection>
-[[Category: Human]]
+[[Category: Homo sapiens]]
-[[Category: Maeda, K]]
+[[Category: Large Structures]]
-[[Category: Maeda, Y]]
+[[Category: Maeda K]]
-[[Category: Takeda, S]]
+[[Category: Maeda Y]]
-[[Category: Yamashita, A]]
+[[Category: Takeda S]]
-[[Category: Ca2+ binding protein]]
+[[Category: Yamashita A]]
-[[Category: Coiled-coil]]
-[[Category: Contractile protein]]
-[[Category: Ef-hand]]
-[[Category: Muscle regulation]]
-[[Category: Thin filament]]