2kkq - Revision history

OCA at 06:46, 1 May 2024

OCA — Wed, 01 May 2024 06:46:26 GMT

←Older revision		Revision as of 06:46, 1 May 2024
Line 1:		Line 1:

	==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==		==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==
-	<StructureSection load='2kkq' size='340' side='right'caption='[[2kkq~~]], [[NMR_Ensembles_of_Models \| 20 NMR models~~]]' scene=''>	+	<StructureSection load='2kkq' size='340' side='right'caption='[[2kkq]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
-	</td></tr><tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat"~~>MYOT, TTID ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&~~id=~~9606 HUMAN])~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [https://pdbe.org/2kkq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [https://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2kkq ProSAT], [https://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [https://pdbe.org/2kkq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [https://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2kkq ProSAT], [https://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[https://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[https://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[https://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>	+	[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[https://omim.org/entry/159000 159000]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[https://omim.org/entry/609200 609200]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[https://omim.org/entry/182920 182920]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>	+	[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 28:		Line 28:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Acton~~, T B~~]]	+	[[Category: Acton TB]]
-	[[Category: Ciccosanti, C]]	+	[[Category: Ciccosanti C]]
-	[[Category: Everett~~, J K~~]]	+	[[Category: Everett JK]]
-	[[Category: Hamilton, K]]	+	[[Category: Hamilton K]]
-	[[Category: Montelione~~, G T]]~~	+	[[Category: Montelione GT]]
-	~~[[Category: Structural genomic~~]]	+	[[Category: Nair R]]
-	[[Category: Nair, R]]	+	[[Category: Rossi P]]
-	[[Category: Rossi, P]]	+	[[Category: Rost B]]
-	[[Category: Rost, B]]	+	[[Category: Shastry R]]
-	[[Category: Shastry, R]]	+	[[Category: Swapna GVT]]
-	[[Category: Swapna~~, G V.T~~]]	+	[[Category: Xiao R]]
-	[[Category: Xiao, R]]	+
-	~~[[Category: Actin-binding]]~~	+
-	~~[[Category: Cell membrane]]~~	+
-	~~[[Category: Cytoplasm]]~~	+
-	~~[[Category: Cytoskeleton]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Immunoglobulin domain]]~~	+
-	~~[[Category: Limb-girdle muscular dystrophy]]~~	+
-	~~[[Category: Membrane]]~~	+
-	~~[[Category: Muscle protein]]~~	+
-	~~[[Category: Nesg]]~~	+
-	~~[[Category: Polymorphism]]~~	+
-	~~[[Category: PSI, Protein structure initiative]]~~	+
-	~~[[Category: Structural protein]]~~	+
-	~~[[Category: Unknown function~~]]	+

OCA at 07:06, 1 December 2021

OCA — Wed, 01 Dec 2021 07:06:50 GMT

←Older revision		Revision as of 07:06, 1 December 2021
Line 3:		Line 3:
	<StructureSection load='2kkq' size='340' side='right'caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2kkq' size='340' side='right'caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
-	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [~~http~~://pdbe.org/2kkq PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2kkq ProSAT], [~~http~~://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [https://pdbe.org/2kkq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [https://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2kkq ProSAT], [https://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[~~http~~://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[~~http~~://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[~~http~~://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>	+	[[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[https://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[https://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[https://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>	+	[[https://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]

OCA at 09:38, 26 February 2020

OCA — Wed, 26 Feb 2020 09:38:44 GMT

←Older revision		Revision as of 09:38, 26 February 2020
Line 1:		Line 1:

	==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==		==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==
-	<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>	+	<StructureSection load='2kkq' size='340' side='right'caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>		<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
Line 29:		Line 29:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Acton, T B]]		[[Category: Acton, T B]]
	[[Category: Ciccosanti, C]]		[[Category: Ciccosanti, C]]

OCA at 07:58, 25 July 2018

OCA — Wed, 25 Jul 2018 07:58:45 GMT

←Older revision		Revision as of 07:58, 25 July 2018
Line 1:		Line 1:
		+
	==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==		==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==
	<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
Line 4:		Line 5:
	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>		<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://pdbe.org/2kkq PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://pdbe.org/2kkq PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2kkq ProSAT], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 14:		Line 15:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kk/2kkq_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kk/2kkq_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: Actin-binding]]		[[Category: Actin-binding]]
	[[Category: Cell membrane]]		[[Category: Cell membrane]]
		+	[[Category: Cytoplasm]]
	[[Category: Cytoskeleton]]		[[Category: Cytoskeleton]]
	[[Category: Disease mutation]]		[[Category: Disease mutation]]
Line 49:		Line 51:
	[[Category: Muscle protein]]		[[Category: Muscle protein]]
	[[Category: Nesg]]		[[Category: Nesg]]
		+	[[Category: Polymorphism]]
	[[Category: PSI, Protein structure initiative]]		[[Category: PSI, Protein structure initiative]]
	[[Category: Structural protein]]		[[Category: Structural protein]]
	[[Category: Unknown function]]		[[Category: Unknown function]]

OCA at 12:54, 9 February 2016

OCA — Tue, 09 Feb 2016 12:54:59 GMT

←Older revision		Revision as of 12:54, 9 February 2016
Line 18:		Line 18:
	<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=2kkq ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>

OCA at 22:27, 10 September 2015

OCA — Thu, 10 Sep 2015 22:27:26 GMT

←Older revision		Revision as of 22:27, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
-	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://pdbe.org/2kkq PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 27:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Acton, T B]]		[[Category: Acton, T B]]
	[[Category: Ciccosanti, C]]		[[Category: Ciccosanti, C]]

OCA at 13:28, 19 January 2015

OCA — Mon, 19 Jan 2015 13:28:48 GMT

←Older revision		Revision as of 13:28, 19 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>		<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>	+	</td></tr><tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[http://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[http://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[http://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>		[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[http://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[http://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[http://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>
Line 28:		Line 28:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Acton, T B.]]	+	[[Category: Acton, T B]]
-	[[Category: Ciccosanti, C.]]	+	[[Category: Ciccosanti, C]]
-	[[Category: Everett, J K.]]	+	[[Category: Everett, J K]]
-	[[Category: Hamilton, K.]]	+	[[Category: Hamilton, K]]
-	[[Category: Montelione, G T.]]	+	[[Category: Montelione, G T]]
-	[[Category: ~~NESG, Northeast~~ Structural ~~Genomics Consortium.~~]]	+	[[Category: Structural genomic]]
-	[[Category: Nair, R.]]	+	[[Category: Nair, R]]
-	[[Category: Rossi, P.]]	+	[[Category: Rossi, P]]
-	[[Category: Rost, B.]]	+	[[Category: Rost, B]]
-	[[Category: Shastry, R.]]	+	[[Category: Shastry, R]]
-	[[Category: Swapna, G V.T.]]	+	[[Category: Swapna, G V.T]]
-	[[Category: Xiao, R.]]	+	[[Category: Xiao, R]]
	[[Category: Actin-binding]]		[[Category: Actin-binding]]
	[[Category: Cell membrane]]		[[Category: Cell membrane]]
Line 49:		Line 49:
	[[Category: Muscle protein]]		[[Category: Muscle protein]]
	[[Category: Nesg]]		[[Category: Nesg]]
-	[[Category: ~~Northeast structural genomics consortium]]~~	+	[[Category: PSI, Protein structure initiative]]
-	~~[[Category:~~ Protein structure initiative]]	+
-	~~[[Category: Psi-2]]~~	+
-	~~[[Category: Structural genomic~~]]	+
	[[Category: Structural protein]]		[[Category: Structural protein]]
	[[Category: Unknown function]]		[[Category: Unknown function]]

OCA at 07:50, 30 September 2014

OCA — Tue, 30 Sep 2014 07:50:38 GMT

←Older revision		Revision as of 07:50, 30 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2kkq\| PDB=2kkq \| SCENE= }}~~	+	==Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.==
-	===Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.===	+	<StructureSection load='2kkq' size='340' side='right' caption='[[2kkq]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
-		+	== Structural highlights ==
-	==Disease==	+	<table><tr><td colspan='2'>[[2kkq]] 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=2KKQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2KKQ FirstGlance]. <br>
-	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[http://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref><ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[http://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[http://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>	+	</td></tr><tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYOT, TTID ([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=2kkq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2kkq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2kkq RCSB], [http://www.ebi.ac.uk/pdbsum/2kkq PDBsum], [http://www.topsan.org/Proteins/NESGC/2kkq TOPSAN]</span></td></tr>
-	==Function==	+	<table>
-	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>	+	== Disease ==
-		+	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[http://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref> <ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[http://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[http://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>
-	==~~About this Structure~~==	+	== Function ==
-	[[~~2kkq~~]] ~~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=~~2KKQ OCA~~].	+	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>
		+	== 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/kk/2kkq_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>

	==See Also==		==See Also==
	*[[Myotilin\|Myotilin]]		*[[Myotilin\|Myotilin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Acton, T B.]]		[[Category: Acton, T B.]]

OCA at 09:17, 24 March 2013

OCA — Sun, 24 Mar 2013 09:17:12 GMT

←Older revision		Revision as of 09:17, 24 March 2013
Line 1:		Line 1:
-	[[Image:2kkq.png\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_2kkq", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_2kkq\| PDB=2kkq \| SCENE= }}		{{STRUCTURE_2kkq\| PDB=2kkq \| SCENE= }}
-
	===Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.===		===Solution NMR Structure of the Ig-like C2-type 2 Domain of Human Myotilin. Northeast Structural Genomics Target HR3158.===

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Defects in MYOT are the cause of limb-girdle muscular dystrophy type 1A (LGMD1A) [MIM:[http://omim.org/entry/159000 159000]]. LGMD1A is an autosomal dominant degenerative myopathy with onset within a mean age of 28 years. LGMD1A is characterized by progressive skeletal muscle weakness of the hip and shoulder girdles, later progressing to include distal weakness, as well as a distinctive dysarthric pattern of speech. Affected muscle exhibits disorganization and streaming of the Z-line.<ref>PMID:10958653</ref><ref>PMID:12428213</ref> Defects in MYOT are the cause of myopathy myofibrillar type 3 (MFM3) [MIM:[http://omim.org/entry/609200 609200]]. A neuromuscular disorder characterized by progressive skeletal muscle weakness greater distally than proximally, tight heel cords, hyporeflexia, cardiomyopathy and peripheral neuropathy in some patients. Affected muscle exhibits disorganization and streaming of the Z-line, presence of large hyaline structures, excessive accumulation of myotilin and other ectopically expressed proteins and prominent congophilic deposits.<ref>PMID:15111675</ref> Defects in MYOT are the cause of spheroid body myopathy (SBM) [MIM:[http://omim.org/entry/182920 182920]]. SBM is an autosomal dominant form of myofibrillar myopathy (MFM), characterized by slowly progressing proximal muscle weakness and dysarthric nasal speech. There is no evidence of cardiomyopathy. Muscle biopsy shows spheroid bodies within the type I muscle fibers.<ref>PMID:16380616</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/MYOTI_HUMAN MYOTI_HUMAN]] Component of a complex of multiple actin cross-linking proteins. Involved in the control of myofibril assembly and stability at the Z lines in muscle cells.<ref>PMID:12499399</ref>

	==About this Structure==		==About this Structure==
Line 16:		Line 12:

	==See Also==		==See Also==
-	*[[~~Group:MUZIC:~~Myotilin\|~~MUZIC:~~Myotilin]]	+	*[[Myotilin\|Myotilin]]
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Acton, T B.]]		[[Category: Acton, T B.]]

OCA at 07:57, 1 April 2012

OCA — Sun, 01 Apr 2012 07:57:26 GMT

←Older revision		Revision as of 07:57, 1 April 2012
Line 16:		Line 16:

	==See Also==		==See Also==
-	*[[Group:MUZIC:Myotilin]]	+	*[[Group:MUZIC:Myotilin\|MUZIC:Myotilin]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Acton, T B.]]		[[Category: Acton, T B.]]