1ip5 - Revision history

OCA at 23:34, 27 December 2023

OCA — Wed, 27 Dec 2023 23:34:31 GMT

←Older revision		Revision as of 23:34, 27 December 2023
Line 3:		Line 3:
	<StructureSection load='1ip5' size='340' side='right'caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1ip5' size='340' side='right'caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=NA:SODIUM+ION'>NA</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]] 1.8Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~><div style='overflow: auto; max-height: 3em;'>[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</div></td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
-	~~<tr~~ id~~='activity'><td class~~="~~sblockLbl~~"><~~b>Activity:</b></td><td class~~=~~"sblockDat"><span class~~=~~'plainlinks~~'>~~[https://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17]~~ </~~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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [https://pdbe.org/1ip5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [https://www.ebi.ac.uk/pdbsum/1ip5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1ip5 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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [https://pdbe.org/1ip5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [https://www.ebi.ac.uk/pdbsum/1ip5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1ip5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[https://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>	+	[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[https://omim.org/entry/105200 105200]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.	+	[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 39:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: Lysozyme]]~~	+	[[Category: Takano K]]
-	[[Category: Takano, K]]	+	[[Category: Yamagata Y]]
-	[[Category: Yamagata, Y]]	+	[[Category: Yutani K]]
-	[[Category: Yutani, K]]	+
-	~~[[Category: Bacteriolytic enzyme]]~~	+
-	~~[[Category: Glycosidase]]~~	+
-	~~[[Category: Hydrolase~~]]	+

OCA at 07:12, 14 April 2021

OCA — Wed, 14 Apr 2021 07:12:57 GMT

OCA at 07:10, 10 July 2019

OCA — Wed, 10 Jul 2019 07:10:53 GMT

←Older revision		Revision as of 07:10, 10 July 2019
Line 1:		Line 1:

	==G105A HUMAN LYSOZYME==		==G105A HUMAN LYSOZYME==
-	<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>	+	<StructureSection load='1ip5' size='340' side='right'caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>		<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
Line 17:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ip/1ip5_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ip/1ip5_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 40:		Line 40:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Lysozyme]]		[[Category: Lysozyme]]
	[[Category: Takano, K]]		[[Category: Takano, K]]

OCA at 09:42, 4 October 2017

OCA — Wed, 04 Oct 2017 09:42:13 GMT

←Older revision		Revision as of 09:42, 4 October 2017
Line 1:		Line 1:
		+
	==G105A HUMAN LYSOZYME==		==G105A HUMAN LYSOZYME==
	<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
Line 6:		Line 7:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://pdbe.org/1ip5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://pdbe.org/1ip5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1ip5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	<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=1ip5 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 23:11, 11 September 2015

OCA — Fri, 11 Sep 2015 23:11:44 GMT

←Older revision		Revision as of 23:11, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://pdbe.org/1ip5 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 30:		Line 30:
	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 1ip5" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 37:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Lysozyme]]		[[Category: Lysozyme]]
	[[Category: Takano, K]]		[[Category: Takano, K]]

OCA at 09:30, 2 January 2015

OCA — Fri, 02 Jan 2015 09:30:28 GMT

←Older revision		Revision as of 09:30, 2 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>		<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>
-	<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>		[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>
Line 39:		Line 39:
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Lysozyme]]		[[Category: Lysozyme]]
-	[[Category: Takano, K.]]	+	[[Category: Takano, K]]
-	[[Category: Yamagata, Y.]]	+	[[Category: Yamagata, Y]]
-	[[Category: Yutani, K.]]	+	[[Category: Yutani, K]]
	[[Category: Bacteriolytic enzyme]]		[[Category: Bacteriolytic enzyme]]
	[[Category: Glycosidase]]		[[Category: Glycosidase]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 15:36, 29 September 2014

OCA — Mon, 29 Sep 2014 15:36:06 GMT

←Older revision		Revision as of 15:36, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1ip5~~\| ~~PDB~~=1ip5 \| ~~SCENE~~= }}	+	==G105A HUMAN LYSOZYME==
-	===~~G105A HUMAN LYSOZYME~~===	+	<StructureSection load='1ip5' size='340' side='right' caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
-	~~{{ABSTRACT_PUBMED_11599030}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>
		+	<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [http://www.ebi.ac.uk/pdbsum/1ip5 PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.
		+	== 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/ip/1ip5_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 ==
		+	Our previous study of six non-Gly to Gly/Ala mutant human lysozymes in a left-handed helical region showed that only one non-Gly residue at a rigid site had unfavorable strain energy as compared with Gly at the same position (Takano et al., Proteins 2001; 44:233-243). To further examine the role of left-handed residues in the conformational stability of a protein, we constructed ten Gly to Ala mutant human lysozymes. Most Gly residues in human lysozyme are located in the left-handed helix region. The thermodynamic parameters for denaturation and crystal structures were determined by differential scanning calorimetry and X-ray analysis, respectively. The difference in denaturation Gibbs energy (DeltaDeltaG) for the ten Gly to Ala mutants ranged from + 1.9 to -7.5 kJ/mol, indicating that the effect of the mutation depends on the environment of the residue. We confirm that Gly in a left-handed region is more favorable at rigid sites than non-Gly, but there is little difference in energetic cost between Gly and non-Gly at flexible sites. The present results indicate that dihedral angles in the backbone conformation and also the flexibility at the position should be considered for analyses of protein stability, and protein structural determination, prediction, and design.

-	~~==Disease==~~	+	Role of amino acid residues in left-handed helical conformation for the conformational stability of a protein.,Takano K, Yamagata Y, Yutani K Proteins. 2001 Nov 15;45(3):274-80. PMID:11599030<ref>PMID:11599030</ref>
-	~~[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects~~ in ~~LYZ are a cause~~ of ~~amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is~~ a ~~hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids~~. ~~Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome~~, ~~arterial hypertension~~, ~~hepatosplenomegaly~~, ~~cholestasis, petechial skin rash~~.<ref>PMID:~~8464497~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www~~.~~uniprot~~.~~org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity~~ of ~~immunoagents~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[1ip5]] 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=1IP5 OCA].~~	+

	==See Also==		==See Also==
-	*[[~~Hen Egg-White (HEW)~~ Lysozyme\|~~Hen Egg-White (HEW)~~ Lysozyme]]	+	*[[Lysozyme 3D structures\|Lysozyme 3D structures]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:011599030</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Lysozyme]]		[[Category: Lysozyme]]

OCA at 02:37, 25 March 2013

OCA — Mon, 25 Mar 2013 02:37:23 GMT

←Older revision		Revision as of 02:37, 25 March 2013
Line 1:		Line 1:
-	[[Image:1ip5.png\|left\|200px]]
-
	{{STRUCTURE_1ip5\| PDB=1ip5 \| SCENE= }}		{{STRUCTURE_1ip5\| PDB=1ip5 \| SCENE= }}
-
	===G105A HUMAN LYSOZYME===		===G105A HUMAN LYSOZYME===
		+	{{ABSTRACT_PUBMED_11599030}}

-	~~{{ABSTRACT_PUBMED_11599030}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:011599030</ref><references group="xtra"/>	+	<ref group="xtra">PMID:011599030</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Lysozyme]]		[[Category: Lysozyme]]

OCA at 21:22, 20 October 2012

OCA — Sat, 20 Oct 2012 21:22:38 GMT

←Older revision		Revision as of 21:22, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[1ip5]] is a 1 chain structure ~~of [[Hen Egg-White (HEW) Lysozyme]]~~ 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=1IP5 OCA].	+	[[1ip5]] 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=1IP5 OCA].

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

OCA: Protected "1ip5" [edit=sysop:move=sysop]

OCA — Fri, 27 Jul 2012 13:04:00 GMT

Protected "1ip5" [edit=sysop:move=sysop]

←Older revision

Revision as of 13:04, 27 July 2012

←Older revision		Revision as of 07:12, 14 April 2021
Line 3:		Line 3:
	<StructureSection load='1ip5' size='340' side='right'caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1ip5' size='340' side='right'caption='[[1ip5]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1ip5]] 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=1IP5 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1IP5 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1gdw\|1gdw]], [[1ip1\|1ip1]], [[1ip2\|1ip2]], [[1ip3\|1ip3]], [[1ip4\|1ip4]], [[1ip6\|1ip6]], [[1ip7\|1ip7]]</div></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [~~http~~://pdbe.org/1ip5 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1ip5 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1ip5 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=1ip5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1ip5 OCA], [https://pdbe.org/1ip5 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1ip5 RCSB], [https://www.ebi.ac.uk/pdbsum/1ip5 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1ip5 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[~~http~~://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>	+	[[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[https://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.	+	[[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]