2n10 - Revision history

OCA at 06:13, 15 May 2024

2024-05-15T06:13:11Z

←Older revision		Revision as of 06:13, 15 May 2024
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
-	</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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 09:52, 14 June 2023

2023-06-14T09:52:36Z

←Older revision		Revision as of 09:52, 14 June 2023
Line 1:		Line 1:

	==Solution structure of MyUb (1080-1131) of human Myosin VI==		==Solution structure of MyUb (1080-1131) of human Myosin VI==
-	<StructureSection load='2n10' size='340' side='right'caption='[[2n10~~]], [[NMR_Ensembles_of_Models \| 20 NMR models~~]]' scene=''>	+	<StructureSection load='2n10' size='340' side='right'caption='[[2n10]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]], [[6e5n\|6e5n]]</div></td></tr>	+	</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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYO6, KIAA0389 ([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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.	+	[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>	+	[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 23:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Ehlinger, A]]	+	[[Category: Ehlinger A]]
-	[[Category: He, F]]	+	[[Category: He F]]
-	[[Category: Walters, K]]	+	[[Category: Walters K]]
-	~~[[Category: Motor protein]]~~	+
-	~~[[Category: Protein transport~~]]	+

OCA at 18:05, 20 October 2021

2021-10-20T18:05:32Z

←Older revision		Revision as of 18:05, 20 October 2021
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</div></td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]], [[6e5n\|6e5n]]</div></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYO6, KIAA0389 ([https://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">MYO6, KIAA0389 ([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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>

OCA at 15:24, 2 June 2021

2021-06-02T15:24:54Z

←Older revision		Revision as of 15:24, 2 June 2021
Line 1:		Line 1:

	==Solution structure of MyUb (1080-1131) of human Myosin VI==		==Solution structure of MyUb (1080-1131) of human Myosin VI==
-	<StructureSection load='2n10' size='340' side='right' caption='[[2n10]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>	+	<StructureSection load='2n10' size='340' side='right'caption='[[2n10]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2N10 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYO6, KIAA0389 ([~~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">MYO6, KIAA0389 ([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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [~~http~~://pdbe.org/2n10 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [https://pdbe.org/2n10 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [https://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.	+	[[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>	+	[[https://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 26:		Line 26:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Ehlinger, A]]		[[Category: Ehlinger, A]]
	[[Category: He, F]]		[[Category: He, F]]

OCA at 17:02, 15 August 2018

2018-08-15T17:02:05Z

←Older revision		Revision as of 17:02, 15 August 2018
Line 3:		Line 3:
	<StructureSection load='2n10' size='340' side='right' caption='[[2n10]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2n10' size='340' side='right' caption='[[2n10]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2n10]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2N10 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2N10 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2n10]] 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=2N10 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [http://pdbe.org/2n10 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [http://www.ebi.ac.uk/pdbsum/2n10 PDBsum]</span></td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">MYO6, KIAA0389 ([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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [http://pdbe.org/2n10 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [http://www.ebi.ac.uk/pdbsum/2n10 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2n10 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 24:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Ehlinger, A]]		[[Category: Ehlinger, A]]
	[[Category: He, F]]		[[Category: He, F]]

OCA at 18:12, 10 May 2016

2016-05-10T18:12:25Z

←Older revision		Revision as of 18:12, 10 May 2016
Line 11:		Line 11:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>		[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Myosin VI is critical for cargo trafficking and sorting during early endocytosis and autophagosome maturation, and abnormalities in these processes are linked to cancers, neurodegeneration, deafness, and hypertropic cardiomyopathy. We identify a structured domain in myosin VI, myosin VI ubiquitin-binding domain (MyUb), that binds to ubiquitin chains, especially those linked via K63, K11, and K29. Herein, we solve the solution structure of MyUb and MyUb:K63-linked diubiquitin. MyUb folds as a compact helix-turn-helix-like motif and nestles between the ubiquitins of K63-linked diubiquitin, interacting with distinct surfaces of each. A nine-amino-acid extension at the C-terminal helix (Helix2) of MyUb is required for myosin VI interaction with endocytic and autophagic adaptors. Structure-guided mutations revealed that a functional MyUb is necessary for optineurin interaction. In addition, we found that an isoform-specific helix restricts MyUb binding to ubiquitin chains. This work provides fundamental insights into myosin VI interaction with ubiquitinated cargo and functional adaptors.
		+
		+	Myosin VI Contains a Compact Structural Motif that Binds to Ubiquitin Chains.,He F, Wollscheid HP, Nowicka U, Biancospino M, Valentini E, Ehlinger A, Acconcia F, Magistrati E, Polo S, Walters KJ Cell Rep. 2016 Mar 22;14(11):2683-94. doi: 10.1016/j.celrep.2016.01.079. Epub, 2016 Mar 10. PMID:26971995<ref>PMID:26971995</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 2n10" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 03:44, 10 March 2016

2016-03-10T03:44:46Z

←Older revision		Revision as of 03:44, 10 March 2016
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-	'''Unreleased structure'''

-	~~The entry~~ 2n10 is ~~ON HOLD until Paper Publication~~	+	==Solution structure of MyUb (1080-1131) of human Myosin VI==
-		+	<StructureSection load='2n10' size='340' side='right' caption='[[2n10]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
-	~~Authors~~: He, F., ~~Ehlinger~~, A., ~~Walters, K~~.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[2n10]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2N10 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2N10 FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2n0z\|2n0z]], [[2n11\|2n11]], [[2n12\|2n12]], [[2n13\|2n13]]</td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<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=2n10 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2n10 OCA], [http://pdbe.org/2n10 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2n10 RCSB], [http://www.ebi.ac.uk/pdbsum/2n10 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Ehlinger, A]]
	[[Category: He, F]]		[[Category: He, F]]
	[[Category: Walters, K]]		[[Category: Walters, K]]
-	[[Category: ~~Ehlinger, A~~]]	+	[[Category: Motor protein]]
		+	[[Category: Protein transport]]

OCA at 07:42, 22 April 2015

2015-04-22T07:42:48Z

←Older revision		Revision as of 07:42, 22 April 2015
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	Authors: He, F., Ehlinger, A., Walters, K.		Authors: He, F., Ehlinger, A., Walters, K.

-	Description: ~~Solution structure of MyUb (1080-1131) of human Myosin VI~~	+	Description:
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
	[[Category: He, F]]		[[Category: He, F]]
	[[Category: Walters, K]]		[[Category: Walters, K]]
	[[Category: Ehlinger, A]]		[[Category: Ehlinger, A]]

OCA at 07:23, 15 April 2015

2015-04-15T07:23:54Z

←Older revision		Revision as of 07:23, 15 April 2015
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 2n10 is ON HOLD	+	The entry 2n10 is ON HOLD until Paper Publication

-	Authors: He, F., Walters, K.	+	Authors: He, F., Ehlinger, A., Walters, K.

	Description: Solution structure of MyUb (1080-1131) of human Myosin VI		Description: Solution structure of MyUb (1080-1131) of human Myosin VI
Line 9:		Line 9:
	[[Category: He, F]]		[[Category: He, F]]
	[[Category: Walters, K]]		[[Category: Walters, K]]
		+	[[Category: Ehlinger, A]]

OCA: Protected "2n10" [edit=sysop:move=sysop]

2015-04-01T07:46:03Z

Protected "2n10" [edit=sysop:move=sysop]

←Older revision

Revision as of 07:46, 1 April 2015