1b1i - Revision history

OCA at 05:34, 9 August 2023

OCA — Wed, 09 Aug 2023 05:34:55 GMT

←Older revision		Revision as of 05:34, 9 August 2023
Line 3:		Line 3:
	<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1B1I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=CIT:CITRIC+ACID'>CIT</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='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [https://pdbe.org/1b1i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [https://www.ebi.ac.uk/pdbsum/1b1i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1b1i 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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [https://pdbe.org/1b1i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [https://www.ebi.ac.uk/pdbsum/1b1i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1b1i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[https://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>	+	[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[https://omim.org/entry/611895 611895]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</ref>	+	[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 31:		Line 31:
	</div>		</div>
	<div class="pdbe-citations 1b1i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 1b1i" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Ribonuclease 3D structures\|Ribonuclease 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Acharya~~, K R~~]]	+	[[Category: Acharya KR]]
-	[[Category: Leonidas~~, D D]]~~	+	[[Category: Leonidas DD]]
-	~~[[Category: Hydrolase~~]]	+

OCA at 09:16, 29 September 2021

OCA — Wed, 29 Sep 2021 09:16:38 GMT

OCA at 09:27, 25 December 2019

OCA — Wed, 25 Dec 2019 09:27:51 GMT

←Older revision		Revision as of 09:27, 25 December 2019
Line 3:		Line 3:
	<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1b1i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>
Line 35:		Line 35:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Acharya, K R]]		[[Category: Acharya, K R]]
	[[Category: Leonidas, D D]]		[[Category: Leonidas, D D]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 08:34, 21 May 2019

OCA — Tue, 21 May 2019 08:34:53 GMT

←Older revision		Revision as of 08:34, 21 May 2019
Line 1:		Line 1:

	==CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN==		==CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN==
-	<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>	+	<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1b1i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>		<table><tr><td colspan='2'>[[1b1i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
Line 16:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/b1/1b1i_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/b1/1b1i_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 35:		Line 35:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Acharya, K R]]		[[Category: Acharya, K R]]
	[[Category: Leonidas, D D]]		[[Category: Leonidas, D D]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 06:02, 17 August 2017

OCA — Thu, 17 Aug 2017 06:02:28 GMT

←Older revision		Revision as of 06:02, 17 August 2017
Line 1:		Line 1:
		+
	==CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN==		==CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN==
	<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1b1i]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://pdbe.org/1b1i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i 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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://pdbe.org/1b1i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1b1i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	<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=1b1i ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 34:		Line 35:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: Human]]
	[[Category: Acharya, K R]]		[[Category: Acharya, K R]]
	[[Category: Leonidas, D D]]		[[Category: Leonidas, D D]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 01:16, 12 September 2015

OCA — Sat, 12 Sep 2015 01:16:13 GMT

←Older revision		Revision as of 01:16, 12 September 2015
Line 2:		Line 2:
	<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i 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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://pdbe.org/1b1i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 29:		Line 29:
	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 1b1i" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Acharya, K R]]		[[Category: Acharya, K R]]
	[[Category: Leonidas, D D]]		[[Category: Leonidas, D D]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 15:31, 15 February 2015

OCA — Sun, 15 Feb 2015 15:31:59 GMT

←Older revision		Revision as of 15:31, 15 February 2015
Line 29:		Line 29:
	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>
-
-	==See Also==
-	*[[User:Jaime.Prilusky/Test/tree\|User:Jaime.Prilusky/Test/tree]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 10:31, 22 December 2014

OCA — Mon, 22 Dec 2014 10:31:16 GMT

←Older revision		Revision as of 10:31, 22 December 2014
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>		<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>	+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i 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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>		[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>
Line 31:		Line 31:

	==See Also==		==See Also==
-	*[[~~Ribonuclease~~\|~~Ribonuclease~~]]	+	*[[User:Jaime.Prilusky/Test/tree\|User:Jaime.Prilusky/Test/tree]]
	== References ==		== References ==
	<references/>		<references/>
Line 37:		Line 37:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Acharya, K R.]]	+	[[Category: Acharya, K R]]
-	[[Category: Leonidas, D D.]]	+	[[Category: Leonidas, D D]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 16:47, 29 September 2014

OCA — Mon, 29 Sep 2014 16:47:33 GMT

←Older revision		Revision as of 16:47, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1b1i~~\| ~~PDB~~=1b1i \| ~~SCENE~~= }}	+	==CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN==
-	===~~CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN~~===	+	<StructureSection load='1b1i' size='340' side='right' caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
-	~~{{ABSTRACT_PUBMED_9918722}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [http://www.ebi.ac.uk/pdbsum/1b1i PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</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/b1/1b1i_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 ==
		+	Human angiogenin (Ang), an unusual member of the pancreatic RNase superfamily, is a potent inducer of angiogenesis in vivo. Its ribonucleolytic activity is weak (10(4) to 10(6)-fold lower than that of bovine RNase A), but nonetheless seems to be essential for biological function. Ang has been implicated in the establishment of a wide range of human tumours and has therefore emerged as an important target for the design of new anti-cancer compounds. We report high-resolution crystal structures for native Ang in two different forms (Pyr1 at 1.8 A and Met-1 at 2.0 A resolution) and for two active-site variants, K40Q and H13A, at 2.0 A resolution. The native structures, together with earlier mutational and biochemical data, provide a basis for understanding the unique functional properties of this molecule. The major structural features that underlie the weakness of angiogenin's RNase activity include: (i) the obstruction of the pyrimidine-binding site by Gln117; (ii) the existence of a hydrogen bond between Thr44 and Thr80 that further suppresses the effectiveness of the pyrimidine site; (iii) the absence of a counterpart for the His119-Asp121 hydrogen bond that potentiates catalysis in RNase A (the corresponding aspartate in Ang, Asp116, has been recruited to stabilise the blockage of the pyrimidine site); and (iv) the absence of any precise structural counterparts for two important purine-binding residues of RNase A. Analysis of the native structures has revealed details of the cell-binding region and nuclear localisation signal of Ang that are critical for angiogenicity. The cell-binding site differs dramatically from the corresponding regions of RNase A and two other homologues, eosinophil-derived neurotoxin and onconase, all of which lack angiogenic activity. Determination of the structures of the catalytically inactive variants K40Q and H13A has now allowed a rigorous assessment of the relationship between the ribonucleolytic and biological activities of Ang. No significant change outside the enzymatic active site was observed in K40Q, establishing that the loss of angiogenic activity for this derivative is directly attributable to disruption of the catalytic apparatus. The H13A structure shows some changes beyond the ribonucleolytic site, but sites involved in cell-binding and nuclear translocation are essentially unaffected by the amino acid replacement.

-	~~==Disease==~~	+	Refined crystal structures of native human angiogenin and two active site variants: implications for the unique functional properties of an enzyme involved in neovascularisation during tumour growth.,Leonidas DD, Shapiro R, Allen SC, Subbarao GV, Veluraja K, Acharya KR J Mol Biol. 1999 Jan 22;285(3):1209-33. PMID:9918722<ref>PMID:9918722</ref>
-	~~[[http~~:~~//www~~.~~uniprot~~.~~org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9~~ (~~ALS9~~) ~~[MIM~~:~~[http://omim~~.~~org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>~~PMID:~~17886298</ref><ref>PMID:15557516</ref><ref>PMID:16501576</ref><ref>PMID:17900154</ref><ref>PMID:18087731</ref>~~<ref>PMID:~~17703939~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as~~ a ~~tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface~~ of ~~endothelial cells; once bound, angiogenin is endocytosed and translocated to~~ the ~~nucleus~~. ~~Angiogenin induces vascularization~~ of ~~normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo~~.<~~ref~~>~~PMID:1400510~~</~~ref~~>~~<ref>PMID:19354288</ref>~~	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[1b1i]] 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=1B1I OCA].	+

	==See Also==		==See Also==
	*[[Ribonuclease\|Ribonuclease]]		*[[Ribonuclease\|Ribonuclease]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:009918722</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Acharya, K R.]]		[[Category: Acharya, K R.]]
	[[Category: Leonidas, D D.]]		[[Category: Leonidas, D D.]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

OCA at 05:23, 25 March 2013

OCA — Mon, 25 Mar 2013 05:23:11 GMT

←Older revision		Revision as of 05:23, 25 March 2013
Line 1:		Line 1:
-	[[Image:1b1i.png\|left\|200px]]
-
	{{STRUCTURE_1b1i\| PDB=1b1i \| SCENE= }}		{{STRUCTURE_1b1i\| PDB=1b1i \| SCENE= }}
-
	===CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN===		===CRYSTAL STRUCTURE OF HUMAN ANGIOGENIN===
		+	{{ABSTRACT_PUBMED_9918722}}

-	~~{{ABSTRACT_PUBMED_9918722}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[http://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref><ref>PMID:15557516</ref><ref>PMID:16501576</ref><ref>PMID:17900154</ref><ref>PMID:18087731</ref><ref>PMID:17703939</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref><ref>PMID:19354288</ref>

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:009918722</ref><references group="xtra"/>	+	<ref group="xtra">PMID:009918722</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Acharya, K R.]]		[[Category: Acharya, K R.]]
	[[Category: Leonidas, D D.]]		[[Category: Leonidas, D D.]]
	[[Category: Hydrolase]]		[[Category: Hydrolase]]

←Older revision		Revision as of 09:16, 29 September 2021
Line 3:		Line 3:
	<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>		<StructureSection load='1b1i' size='340' side='right'caption='[[1b1i]], [[Resolution\|resolution]] 1.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1B1I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1b1i]] 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=1B1I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1B1I FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PCA:PYROGLUTAMIC+ACID'>PCA</scene></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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [~~http~~://pdbe.org/1b1i PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1b1i PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1b1i 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=1b1i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1b1i OCA], [https://pdbe.org/1b1i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1b1i RCSB], [https://www.ebi.ac.uk/pdbsum/1b1i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1b1i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[~~http~~://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>	+	[[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] Defects in ANG are the cause of susceptibility to amyotrophic lateral sclerosis type 9 (ALS9) [MIM:[https://omim.org/entry/611895 611895]]. ALS is a degenerative disorder of motor neurons in the cortex, brain stem and spinal cord. ALS is characterized by muscular weakness and atrophy.<ref>PMID:17886298</ref> <ref>PMID:15557516</ref> <ref>PMID:16501576</ref> <ref>PMID:17900154</ref> <ref>PMID:18087731</ref> <ref>PMID:17703939</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</ref>	+	[[https://www.uniprot.org/uniprot/ANGI_HUMAN ANGI_HUMAN]] May function as a tRNA-specific ribonuclease that abolishes protein synthesis by specifically hydrolyzing cellular tRNAs. Binds to actin on the surface of endothelial cells; once bound, angiogenin is endocytosed and translocated to the nucleus. Angiogenin induces vascularization of normal and malignant tissues. Angiogenic activity is regulated by interaction with RNH1 in vivo.<ref>PMID:1400510</ref> <ref>PMID:19354288</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]