2jt8 - Revision history

OCA at 08:36, 14 June 2023

OCA — Wed, 14 Jun 2023 08:36:58 GMT

←Older revision		Revision as of 08:36, 14 June 2023
Line 1:		Line 1:

	==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==		==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==
-	<StructureSection load='2jt8' size='340' side='right'caption='[[2jt8~~]], [[NMR_Ensembles_of_Models \| 10 NMR models~~]]' scene=''>	+	<StructureSection load='2jt8' size='340' side='right'caption='[[2jt8]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2jt8]] is a 1 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=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
-	</td></tr><tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([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'>[https://proteopedia.org/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [https://pdbe.org/2jt8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [https://www.ebi.ac.uk/pdbsum/2jt8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2jt8 ProSAT]</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=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [https://pdbe.org/2jt8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [https://www.ebi.ac.uk/pdbsum/2jt8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2jt8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[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>	+	[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 ==		== Function ==
-	[[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.	+	[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 ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 33:		Line 32:

	==See Also==		==See Also==
-	*[[Troponin\|Troponin]]	+	*[[Troponin 3D structures\|Troponin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Letourneau, P]]	+	[[Category: Letourneau P]]
-	[[Category: Mercier, P]]	+	[[Category: Mercier P]]
-	[[Category: Sykes~~, B D~~]]	+	[[Category: Sykes BD]]
-	[[Category: Wang, X]]	+	[[Category: Wang X]]
-	~~[[Category: Acetylation]]~~	+
-	~~[[Category: Calcium-bind protein]]~~	+
-	~~[[Category: Ef-hand protein]]~~	+
-	~~[[Category: Muscle protein]]~~	+
-	~~[[Category: Phe-to-trp mutation]]~~	+
-	~~[[Category: Polymorphism]]~~	+
-	~~[[Category: Structural protein~~]]	+

OCA at 17:58, 20 October 2021

OCA — Wed, 20 Oct 2021 17:58:02 GMT

OCA at 06:50, 19 February 2020

OCA — Wed, 19 Feb 2020 06:50:02 GMT

←Older revision		Revision as of 06:50, 19 February 2020
Line 1:		Line 1:

	==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==		==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==
-	<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>	+	<StructureSection load='2jt8' size='340' side='right'caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Letourneau, P]]		[[Category: Letourneau, P]]
	[[Category: Mercier, P]]		[[Category: Mercier, P]]

OCA at 11:05, 18 July 2018

OCA — Wed, 18 Jul 2018 11:05:41 GMT

←Older revision		Revision as of 11:05, 18 July 2018
Line 1:		Line 1:
		+
	==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==		==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==
	<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>		<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://pdbe.org/2jt8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</span></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=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://pdbe.org/2jt8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2jt8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 15:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/jt/2jt8_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/jt/2jt8_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
Line 42:		Line 43:
	[[Category: Sykes, B D]]		[[Category: Sykes, B D]]
	[[Category: Wang, X]]		[[Category: Wang, X]]
		+	[[Category: Acetylation]]
	[[Category: Calcium-bind protein]]		[[Category: Calcium-bind protein]]
	[[Category: Ef-hand protein]]		[[Category: Ef-hand protein]]
	[[Category: Muscle protein]]		[[Category: Muscle protein]]
	[[Category: Phe-to-trp mutation]]		[[Category: Phe-to-trp mutation]]
		+	[[Category: Polymorphism]]
	[[Category: Structural protein]]		[[Category: Structural protein]]

OCA at 08:37, 10 February 2016

OCA — Wed, 10 Feb 2016 08:37:37 GMT

←Older revision		Revision as of 08:37, 10 February 2016
Line 19:		Line 19:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2jt8 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 07:09, 11 September 2015

OCA — Fri, 11 Sep 2015 07:09:51 GMT

←Older revision		Revision as of 07:09, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>		<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</span></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=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://pdbe.org/2jt8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 2jt8" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 36:		Line 37:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Letourneau, P]]		[[Category: Letourneau, P]]
	[[Category: Mercier, P]]		[[Category: Mercier, P]]

OCA at 18:26, 19 January 2015

OCA — Mon, 19 Jan 2015 18:26:32 GMT

←Older revision		Revision as of 18:26, 19 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>	+	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</span></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=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== 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/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>
Line 37:		Line 37:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Letourneau, P.]]	+	[[Category: Letourneau, P]]
-	[[Category: Mercier, P.]]	+	[[Category: Mercier, P]]
-	[[Category: Sykes, B D.]]	+	[[Category: Sykes, B D]]
-	[[Category: Wang, X.]]	+	[[Category: Wang, X]]
	[[Category: Calcium-bind protein]]		[[Category: Calcium-bind protein]]
	[[Category: Ef-hand protein]]		[[Category: Ef-hand protein]]

OCA at 10:48, 30 September 2014

OCA — Tue, 30 Sep 2014 10:48:13 GMT

←Older revision		Revision as of 10:48, 30 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2jt8\| PDB=2jt8 \| SCENE= }}~~	+	==Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C==
-	===Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C===	+	<StructureSection load='2jt8' size='340' side='right' caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>
-	~~{{ABSTRACT_PUBMED_16131667}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [http://www.ebi.ac.uk/pdbsum/2jt8 PDBsum]</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>
		+	== 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.
		+	== 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/jt/2jt8_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	19F NMR spectroscopy is potentially a powerful tool for probing protein properties in situ. However, results obtained using this technique are relevant only if the 19F probe offers minimal perturbation to the surrounding environment. In this paper, we examine the effect of 5-fluorotryptophan (5fW) incorporation on the three-dimensional structure of cardiac troponin-C (cTnC), with the intention of developing a 19F-labeled TnC for use in in situ 19FNMR. We find that, in general, 5fW does not perturb the structure of the protein significantly. Replacement of residue Phe 153 with 5fW produces no noticeable change in protein conformation. However, replacement of residue Phe 104 with 5fW produces a folding behavior that is dependent on the Escherichia coli strain used to express the mutant. The orientations of the indole rings in these mutants are such that the Trp residue adopts a chi2 of approximately 90 degrees in the F104W mutant and approximately -100 degrees in the F153W mutant. Using results from 19F-1H heteronuclear NOE experiment, we show the replacement of L-Trp with 5fW at these positions does not change the orientation of the indole ring and the spread of the 5fW side-chain dihedral angles increases moderately for the F104(5fW) mutant and not at all for the F153(5fW) mutant. Based on these structures, we conclude that the substitution of Phe by 5fW at these two positions has minimal effects on the structure of cTnC and that the 5fW indole rings in both mutants have well defined orientation, making the two mutants viable candidates for use in in situ 19F NMR spectroscopy.

-	~~==Disease==~~	+	Effects of Phe-to-Trp mutation and fluorotryptophan incorporation on the solution structure of cardiac troponin C, and analysis of its suitability as a potential probe for in situ NMR studies.,Wang X, Mercier P, Letourneau PJ, Sykes BD Protein Sci. 2005 Sep;14(9):2447-60. PMID:16131667<ref>PMID:16131667</ref>
-	~~[[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>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[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~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[2jt8]] is a 1 chain structure with sequence from [http:~~/~~/en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA].~~	+

	==See Also==		==See Also==
	*[[Troponin\|Troponin]]		*[[Troponin\|Troponin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:016131667</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Letourneau, P.]]		[[Category: Letourneau, P.]]

OCA at 02:48, 25 March 2013

OCA — Mon, 25 Mar 2013 02:48:26 GMT

←Older revision		Revision as of 02:48, 25 March 2013
Line 1:		Line 1:
-	[[Image:2jt8.png\|left\|200px]]
-
	{{STRUCTURE_2jt8\| PDB=2jt8 \| SCENE= }}		{{STRUCTURE_2jt8\| PDB=2jt8 \| SCENE= }}
-
	===Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C===		===Solution structure of the F153-to-5-flurotryptophan mutant of human cardiac troponin C===
		+	{{ABSTRACT_PUBMED_16131667}}

-	~~{{ABSTRACT_PUBMED_16131667}}~~	+	==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>
		+
		+	==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.

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:016131667</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016131667</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Letourneau, P.]]		[[Category: Letourneau, P.]]

OCA at 17:00, 20 October 2012

OCA — Sat, 20 Oct 2012 17:00:00 GMT

←Older revision		Revision as of 17:00, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[2jt8]] is a 1 chain structure ~~of [[Troponin]]~~ with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA].	+	[[2jt8]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA].

	==See Also==		==See Also==

←Older revision		Revision as of 17:58, 20 October 2021
Line 3:		Line 3:
	<StructureSection load='2jt8' size='340' side='right'caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>		<StructureSection load='2jt8' size='340' side='right'caption='[[2jt8]], [[NMR_Ensembles_of_Models \| 10 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2jt8]] is a 1 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2jt8]] is a 1 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=2JT8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2JT8 FirstGlance]. <br>
	</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>		</td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=FTR:FLUOROTRYPTOPHANE'>FTR</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">TNNC1, TNNC ([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'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [~~http~~://pdbe.org/2jt8 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2jt8 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2jt8 ProSAT]</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=2jt8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2jt8 OCA], [https://pdbe.org/2jt8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2jt8 RCSB], [https://www.ebi.ac.uk/pdbsum/2jt8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2jt8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== 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>	+	[[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 ==		== 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.	+	[[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 ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]