OCA at 07:27, 11 October 2023

OCA — Wed, 11 Oct 2023 07:27:55 GMT

←Older revision		Revision as of 07:27, 11 October 2023
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	==Crystal Structure of Amino Acids 1220-1276 of Human Beta Cardiac Myosin Fused to Gp7 and Eb1==		==Crystal Structure of Amino Acids 1220-1276 of Human Beta Cardiac Myosin Fused to Gp7 and Eb1==
-	<StructureSection load='6pf2' size='340' side='right'caption='[[6pf2]]' scene=''>	+	<StructureSection load='6pf2' size='340' side='right'caption='[[6pf2]], [[Resolution\|resolution]] 2.17Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6PF2 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=6PF2 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6pf2]] is a 2 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=6PF2 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6PF2 FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=6pf2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pf2 OCA], [~~http~~://pdbe.org/6pf2 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6pf2 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6pf2 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6pf2 ProSAT]</span></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]] 2.17Å</td></tr>
		+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</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=6pf2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pf2 OCA], [https://pdbe.org/6pf2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6pf2 RCSB], [https://www.ebi.ac.uk/pdbsum/6pf2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6pf2 ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[https://www.uniprot.org/uniprot/MYH7_HUMAN MYH7_HUMAN] Defects in MYH7 are the cause of familial hypertrophic cardiomyopathy type 1 (CMH1) [MIM:[https://omim.org/entry/192600 192600]. 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:1975517</ref> <ref>PMID:1417858</ref> <ref>PMID:1638703</ref> <ref>PMID:1552912</ref> <ref>PMID:8250038</ref> <ref>PMID:8343162</ref> <ref>PMID:8435239</ref> <ref>PMID:8268932</ref> <ref>PMID:8254035</ref> <ref>PMID:8483915</ref> <ref>PMID:7848441</ref> <ref>PMID:7874131</ref> <ref>PMID:8282798</ref> <ref>PMID:7581410</ref> <ref>PMID:7731997</ref> <ref>PMID:8655135</ref> <ref>PMID:8899546</ref> <ref>PMID:10065021</ref> <ref>PMID:9544842</ref> <ref>PMID:9829907</ref> <ref>PMID:9822100</ref> <ref>PMID:10521296</ref> <ref>PMID:10563488</ref> <ref>PMID:10329202</ref> <ref>PMID:10679957</ref> <ref>PMID:10862102</ref> <ref>PMID:11113006</ref> <ref>PMID:11214007</ref> <ref>PMID:11733062</ref> <ref>PMID:11424919</ref> <ref>PMID:11133230</ref> <ref>PMID:12081993</ref> <ref>PMID:11861413</ref> <ref>PMID:11968089</ref> <ref>PMID:12951062</ref> <ref>PMID:12566107</ref> <ref>PMID:12707239</ref> <ref>PMID:12974739</ref> <ref>PMID:12820698</ref> <ref>PMID:12975413</ref> <ref>PMID:12590187</ref> <ref>PMID:12818575</ref> <ref>PMID:15358028</ref> <ref>PMID:15563892</ref> <ref>PMID:15483641</ref> <ref>PMID:15858117</ref> <ref>PMID:16199542</ref> <ref>PMID:15856146</ref> <ref>PMID:16650083</ref> <ref>PMID:16938236</ref> <ref>PMID:17372140</ref> <ref>PMID:18403758</ref> Defects in MYH7 are the cause of myopathy myosin storage (MYOMS) [MIM:[https://omim.org/entry/608358 608358]. In this disorder, muscle biopsy shows type 1 fiber predominance and increased interstitial fat and connective tissue. Inclusion bodies consisting of the beta cardiac myosin heavy chain are present in the majority of type 1 fibers, but not in type 2 fibers.<ref>PMID:14520662</ref> <ref>PMID:15136674</ref> <ref>PMID:17336526</ref> Defects in MYH7 are the cause of scapuloperoneal myopathy MYH7-related (SPMM) [MIM:[https://omim.org/entry/181430 181430]; also known as scapuloperoneal syndrome myopathic type. SPMM is a progressive muscular atrophia beginning in the lower legs and affecting the shoulder region earlier and more severely than distal arm.<ref>PMID:17336526</ref> Defects in MYH7 are a cause of cardiomyopathy dilated type 1S (CMD1S) [MIM:[https://omim.org/entry/613426 613426]. 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:11106718</ref> <ref>PMID:12379228</ref> <ref>PMID:15769782</ref> <ref>PMID:21846512</ref> Defects in MYH7 are the cause of myopathy distal type 1 (MPD1) [MIM:[https://omim.org/entry/160500 160500]. MPD1 is a muscular disorder characterized by early-onset selective weakness of the great toe and ankle dorsiflexors, followed by weakness of the finger extensors. Mild proximal weakness occasionally develops years later after the onset of the disease.<ref>PMID:15322983</ref> <ref>PMID:17548557</ref>
		+	== Function ==
		+	[https://www.uniprot.org/uniprot/MARE1_HUMAN MARE1_HUMAN] Binds to the plus end of microtubules and regulates the dynamics of the microtubule cytoskeleton. Promotes cytoplasmic microtubule nucleation and elongation. May be involved in spindle function by stabilizing microtubules and anchoring them at centrosomes. May play a role in cell migration.<ref>PMID:12388762</ref> <ref>PMID:21646404</ref> <ref>PMID:16109370</ref> <ref>PMID:19632184</ref> [https://www.uniprot.org/uniprot/MYH7_HUMAN MYH7_HUMAN] Muscle contraction.
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Ajay G]]		[[Category: Ajay G]]

OCA at 06:19, 25 June 2020

OCA — Thu, 25 Jun 2020 06:19:06 GMT

←Older revision		Revision as of 06:19, 25 June 2020
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-	'''Unreleased structure'''

-	~~The entry~~ 6pf2 is ~~ON HOLD until Paper Publication~~	+	==Crystal Structure of Amino Acids 1220-1276 of Human Beta Cardiac Myosin Fused to Gp7 and Eb1==
-		+	<StructureSection load='6pf2' size='340' side='right'caption='[[6pf2]]' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6PF2 OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6PF2 FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=6pf2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6pf2 OCA], [http://pdbe.org/6pf2 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6pf2 RCSB], [http://www.ebi.ac.uk/pdbsum/6pf2 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6pf2 ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	</table>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Ajay G]]
		+	[[Category: Andreas MP]]
		+	[[Category: Cui Q]]
		+	[[Category: Hargreaves M]]
		+	[[Category: Kieffer DJ]]
		+	[[Category: Kirsch CJ]]
		+	[[Category: Korkmaz EN]]
		+	[[Category: Rayment I]]

OCA at 04:14, 7 August 2019

OCA — Wed, 07 Aug 2019 04:14:03 GMT

←Older revision		Revision as of 04:14, 7 August 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6pf2 is ON HOLD	+	The entry 6pf2 is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6pf2" [edit=sysop:move=sysop]

OCA — Wed, 03 Jul 2019 04:14:46 GMT

Protected "6pf2" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:14, 3 July 2019

OCA: New page: '''Unreleased structure''' The entry 6pf2 is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 03 Jul 2019 04:14:45 GMT

New page: '''Unreleased structure''' The entry 6pf2 is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6pf2 is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]

6pf2 - Revision history

OCA at 07:27, 11 October 2023

OCA at 06:19, 25 June 2020

OCA at 04:14, 7 August 2019

OCA: Protected "6pf2" [edit=sysop:move=sysop]

OCA: New page: '''Unreleased structure''' The entry 6pf2 is ON HOLD Authors: Description: Category: Unreleased Structures