2e1e - Revision history

OCA at 08:33, 25 October 2023

2023-10-25T08:33:22Z

← Older revision		Revision as of 08:33, 25 October 2023
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	<StructureSection load='2e1e' size='340' side='right'caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='2e1e' size='340' side='right'caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2E1E FirstGlance]. <br>		<table><tr><td colspan='2'>[[2e1e]] is a 1 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=2E1E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>~~</td></tr>		</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.3Å</td></tr>
	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"><~~div style~~='~~overflow~~: ~~auto; max-height: 3em;~~'>~~[[2e1f\|2e1f]]~~</~~div~~></td></tr>		<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [https://pdbe.org/2e1e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [https://www.ebi.ac.uk/pdbsum/2e1e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2e1e 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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [https://pdbe.org/2e1e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [https://www.ebi.ac.uk/pdbsum/2e1e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2e1e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[https://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500]].		[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[https://omim.org/entry/277700 277700]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500].
	== Function ==		== Function ==
	[[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref> <ref>PMID:17563354</ref> <ref>PMID:18596042</ref> <ref>PMID:19652551</ref> <ref>PMID:19283071</ref>		[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref> <ref>PMID:17563354</ref> <ref>PMID:18596042</ref> <ref>PMID:19652551</ref> <ref>PMID:19283071</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Hakoshima, T]]		[[Category: Hakoshima T]]
	[[Category: Kitano, K]]		[[Category: Kitano K]]
	[[Category: Yoshihara, N]]		[[Category: Yoshihara N]]
	~~[[Category: Hrdc domain]]~~
	~~[[Category: Hydrolase~~]]

OCA at 17:19, 15 December 2021

2021-12-15T17:19:19Z

OCA at 08:25, 11 March 2020

2020-03-11T08:25:19Z

← Older revision		Revision as of 08:25, 11 March 2020
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	==Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN==		==Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN==
	<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='2e1e' size='340' side='right'caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>		<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
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	==See Also==		==See Also==
	*[[Helicase\|Helicase]]		*[[Helicase 3D structures\|Helicase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Hakoshima, T]]		[[Category: Hakoshima, T]]
	[[Category: Kitano, K]]		[[Category: Kitano, K]]

OCA at 06:59, 6 June 2018

2018-06-06T06:59:24Z

← Older revision		Revision as of 06:59, 6 June 2018
Line 1:		Line 1:

	==Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN==		==Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN==
	<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
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	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://pdbe.org/2e1e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e 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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://pdbe.org/2e1e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2e1e 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/e1/2e1e_consurf.spt"</scriptWhenChecked>		<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/e1/2e1e_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>
	</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=2e1e ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 11:31, 11 September 2015

2015-09-11T11:31:37Z

← Older revision		Revision as of 11:31, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>		<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e 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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://pdbe.org/2e1e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e 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 2e1e" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Homo sapiens~~]]		[[Category: Human]]
	[[Category: Hakoshima, T]]		[[Category: Hakoshima, T]]
	[[Category: Kitano, K]]		[[Category: Kitano, K]]

OCA at 18:13, 15 January 2015

2015-01-15T18:13:58Z

← Older revision		Revision as of 18:13, 15 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>		<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene><br>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>
	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e 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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e PDBsum]</span></td></tr>
	<table>		</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[http://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]].		[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[http://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]].
Line 37:		Line 37:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hakoshima, T.]]		[[Category: Hakoshima, T]]
	[[Category: Kitano, K.]]		[[Category: Kitano, K]]
	[[Category: Yoshihara, N.]]		[[Category: Yoshihara, N]]
	[[Category: Hrdc domain]]		[[Category: Hrdc domain]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 01:10, 30 September 2014

2014-09-30T01:10:58Z

← Older revision		Revision as of 01:10, 30 September 2014
Line 1:		Line 1:
	~~{{STRUCTURE_2e1e\| PDB=2e1e \| SCENE= }}~~		==Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN==
	===Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN===		<StructureSection load='2e1e' size='340' side='right' caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	~~{{ABSTRACT_PUBMED_17148451}}~~		== Structural highlights ==
			<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
			</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene><br>
			<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [http://www.ebi.ac.uk/pdbsum/2e1e PDBsum]</span></td></tr>
			<table>
			== Disease ==
			[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[http://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]].
			== Function ==
			[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref> <ref>PMID:17563354</ref> <ref>PMID:18596042</ref> <ref>PMID:19652551</ref> <ref>PMID:19283071</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/e1/2e1e_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 ==
			Werner syndrome is a human premature aging disorder characterized by chromosomal instability. The disease is caused by the functional loss of WRN, a member of the RecQ-helicase family that plays an important role in DNA metabolic pathways. WRN contains four structurally folded domains comprising an exonuclease, a helicase, a winged-helix, and a helicase-and-ribonuclease D/C-terminal (HRDC) domain. In contrast to the accumulated knowledge pertaining to the biochemical functions of the three N-terminal domains, the function of C-terminal HRDC remains unknown. In this study, the crystal structure of the human WRN HRDC domain has been determined. The domain forms a bundle of alpha-helices similar to those of Saccharomyces cerevisiae Sgs1 and Escherichia coli RecQ. Surprisingly, the extra ten residues at each of the N and C termini of the domain were found to participate in the domain architecture by forming an extended portion of the first helix alpha1, and a novel looping motif that traverses straight along the domain surface, respectively. The motifs combine to increase the domain surface of WRN HRDC, which is larger than that of Sgs1 and E. coli. In WRN HRDC, neither of the proposed DNA-binding surfaces in Sgs1 or E. coli is conserved, and the domain was shown to lack DNA-binding ability in vitro. Moreover, the domain was shown to be thermostable and resistant to protease digestion, implying independent domain evolution in WRN. Coupled with the unique long linker region in WRN, the WRN HRDC may be adapted to play a distinct function in WRN that involves protein-protein interactions.

	~~==Disease==~~		Crystal structure of the HRDC domain of human Werner syndrome protein, WRN.,Kitano K, Yoshihara N, Hakoshima T J Biol Chem. 2007 Jan 26;282(4):2717-28. Epub 2006 Dec 4. PMID:17148451<ref>PMID:17148451</ref>
	~~[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause~~ of Werner syndrome (WRN~~) [MIM:[http://omim.org/entry/277700 277700]]~~. ~~WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders~~, ~~including atherosclerosis~~, ~~cancer~~, ~~non~~-~~insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis~~. ~~The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins~~.<ref>PMID:~~16673358~~</ref> ~~Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]].~~

	~~==Function==~~		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	~~[[http:~~/~~/www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with~~ a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of ~~DNA polymerases at~~ the ~~site of DNA lesions~~. ~~Important for genomic integrity~~. ~~Plays a role in the formation~~ of ~~DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity)~~.<~~ref~~>~~PMID:11863428</ref><ref>PMID:17563354~~</~~ref><ref~~>~~PMID:18596042</ref><ref>PMID:19652551</ref><ref>PMID:19283071</ref>~~		</div>

	~~==About this Structure==~~
	[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA].

	==See Also==		==See Also==
	*[[Helicase\|Helicase]]		*[[Helicase\|Helicase]]
			== References ==
	==~~Reference~~==		<references/>
	~~<ref group="xtra">PMID:017148451</ref>~~<references ~~group="xtra"~~/><~~references~~/>		__TOC__
			</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hakoshima, T.]]		[[Category: Hakoshima, T.]]

OCA at 11:24, 24 March 2013

2013-03-24T11:24:28Z

← Older revision		Revision as of 11:24, 24 March 2013
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	~~[[Image:2e1e.png\|left\|200px]]~~

	{{STRUCTURE_2e1e\| PDB=2e1e \| SCENE= }}		{{STRUCTURE_2e1e\| PDB=2e1e \| SCENE= }}
			===Crystal structure of the HRDC Domain of Human Werner Syndrome Protein, WRN===
			{{ABSTRACT_PUBMED_17148451}}

	===~~Crystal structure~~ of the ~~HRDC Domain~~ of ~~Human Werner Syndrome Protein~~, WRN~~===~~		==Disease==
			[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[http://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[http://omim.org/entry/114500 114500]].

	~~{{ABSTRACT_PUBMED_17148451}}~~		==Function==
			[[http://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref><ref>PMID:17563354</ref><ref>PMID:18596042</ref><ref>PMID:19652551</ref><ref>PMID:19283071</ref>

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

	==Reference==		==Reference==
	<ref group="xtra">PMID:017148451</ref><references group="xtra"/>		<ref group="xtra">PMID:017148451</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hakoshima, T.]]		[[Category: Hakoshima, T.]]

OCA at 18:34, 20 October 2012

2012-10-20T18:34:20Z

← Older revision		Revision as of 18:34, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
	[[2e1e]] is a 1 chain structure ~~of [[Helicase]]~~ with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA].		[[2e1e]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA].

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

OCA: Protected "2e1e" [edit=sysop:move=sysop]

2012-07-27T04:30:35Z

Protected "2e1e" [edit=sysop:move=sysop]

← Older revision	Revision as of 04:30, 27 July 2012
(No difference)

← Older revision		Revision as of 17:19, 15 December 2021
Line 3:		Line 3:
	<StructureSection load='2e1e' size='340' side='right'caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='2e1e' size='340' side='right'caption='[[2e1e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2E1E FirstGlance]. <br>		<table><tr><td colspan='2'>[[2e1e]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2E1E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2E1E FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2e1f\|2e1f]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2e1f\|2e1f]]</div></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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [~~http~~://pdbe.org/2e1e PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2e1e PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2e1e 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=2e1e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2e1e OCA], [https://pdbe.org/2e1e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2e1e RCSB], [https://www.ebi.ac.uk/pdbsum/2e1e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2e1e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[[~~http~~://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[~~http~~://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[~~http~~://omim.org/entry/114500 114500]].		[[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Defects in WRN are a cause of Werner syndrome (WRN) [MIM:[https://omim.org/entry/277700 277700]]. WRN is a rare autosomal recessive progeroid syndrome characterized by the premature onset of multiple age-related disorders, including atherosclerosis, cancer, non-insulin-dependent diabetes mellitus, ocular cataracts and osteoporosis. The major cause of death, at a median age of 47, is myocardial infarction. Currently all known WS mutations produces prematurely terminated proteins.<ref>PMID:16673358</ref> Defects in WRN may be a cause of colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500]].
	== Function ==		== Function ==
	[[~~http~~://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref> <ref>PMID:17563354</ref> <ref>PMID:18596042</ref> <ref>PMID:19652551</ref> <ref>PMID:19283071</ref>		[[https://www.uniprot.org/uniprot/WRN_HUMAN WRN_HUMAN]] Multifunctional enzyme that has both magnesium and ATP-dependent DNA-helicase activity and 3'->5' exonuclease activity towards double-stranded DNA with a 5'-overhang. Has no nuclease activity towards single-stranded DNA or blunt-ended double-stranded DNA. Binds preferentially to DNA substrates containing alternate secondary structures, such as replication forks and Holliday junctions. May play an important role in the dissociation of joint DNA molecules that can arise as products of homologous recombination, at stalled replication forks or during DNA repair. Alleviates stalling of DNA polymerases at the site of DNA lesions. Important for genomic integrity. Plays a role in the formation of DNA replication focal centers; stably associates with foci elements generating binding sites for RP-A (By similarity).<ref>PMID:11863428</ref> <ref>PMID:17563354</ref> <ref>PMID:18596042</ref> <ref>PMID:19652551</ref> <ref>PMID:19283071</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]