2fg8 - Revision history

OCA at 09:26, 30 August 2023

OCA — Wed, 30 Aug 2023 09:26:44 GMT

←Older revision		Revision as of 09:26, 30 August 2023
Line 3:		Line 3:
	<StructureSection load='2fg8' size='340' side='right'caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='2fg8' size='340' side='right'caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=CS:CESIUM+ION'>CS</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]] 2.5Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~><div style~~=~~'overflow: auto; max-height: 3em;'~~>~~[[2fg4\|2fg4]], [[2ffx\|2ffx]]~~<~~/div></td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>
-	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td>~~<td class="sblockDat">FTL ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</td></tr>	+
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [https://pdbe.org/2fg8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [https://www.ebi.ac.uk/pdbsum/2fg8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2fg8 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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [https://pdbe.org/2fg8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [https://www.ebi.ac.uk/pdbsum/2fg8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2fg8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[https://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[https://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>	+	[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[https://omim.org/entry/600886 600886]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[https://omim.org/entry/606159 606159]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref> <ref>PMID:20159981</ref>	+	[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref> <ref>PMID:20159981</ref>
	== 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: Carter~~, D C~~]]	+	[[Category: Carter DC]]
-	[[Category: Ellenburg~~, M P~~]]	+	[[Category: Ellenburg MP]]
-	[[Category: Ho~~, J X~~]]	+	[[Category: Ho JX]]
-	[[Category: Li, C]]	+	[[Category: Li C]]
-	[[Category: Ruble~~, J R~~]]	+	[[Category: Ruble JR]]
-	[[Category: Wang~~, Z M]]~~	+	[[Category: Wang ZM]]
-	~~[[Category: Ferritin light chain perdeuterated]]~~	+
-	~~[[Category: Metal binding protein~~]]	+

OCA at 07:16, 24 February 2021

OCA — Wed, 24 Feb 2021 07:16:55 GMT

←Older revision		Revision as of 07:16, 24 February 2021
Line 1:		Line 1:

	==Structure of Human Ferritin L Chain==		==Structure of Human Ferritin L Chain==
-	<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>	+	<StructureSection load='2fg8' size='340' side='right'caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2fg4\|2fg4]], [[2ffx\|2ffx]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [~~http~~://pdbe.org/2fg8 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2fg8 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2fg8 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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [https://pdbe.org/2fg8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [https://www.ebi.ac.uk/pdbsum/2fg8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2fg8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[~~http~~://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[~~http~~://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>	+	[[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[https://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[https://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref> <ref>PMID:20159981</ref>	+	[[https://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref> <ref>PMID:20159981</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 34:		Line 34:

	==See Also==		==See Also==
-	*[[Ferritin\|Ferritin]]	+	*[[Ferritin 3D structures\|Ferritin 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 40:		Line 40:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Carter, D C]]		[[Category: Carter, D C]]
	[[Category: Ellenburg, M P]]		[[Category: Ellenburg, M P]]

OCA at 08:54, 14 June 2018

OCA — Thu, 14 Jun 2018 08:54:59 GMT

←Older revision		Revision as of 08:54, 14 June 2018
Line 1:		Line 1:
		+
	==Structure of Human Ferritin L Chain==		==Structure of Human Ferritin L Chain==
	<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>
Line 6:		Line 7:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://pdbe.org/2fg8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://pdbe.org/2fg8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2fg8 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 16:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/fg/2fg8_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/fg/2fg8_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=2fg8 ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 08:31, 11 September 2015

OCA — Fri, 11 Sep 2015 08:31:08 GMT

←Older revision		Revision as of 08:31, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>		<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://pdbe.org/2fg8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 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 2fg8" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 37:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Carter, D C]]		[[Category: Carter, D C]]
	[[Category: Ellenburg, M P]]		[[Category: Ellenburg, M P]]

OCA at 09:08, 16 January 2015

OCA — Fri, 16 Jan 2015 09:08:35 GMT

←Older revision		Revision as of 09:08, 16 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[http://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[http://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>		[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[http://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[http://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>
Line 38:		Line 38:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Carter, D C.]]	+	[[Category: Carter, D C]]
-	[[Category: Ellenburg, M P.]]	+	[[Category: Ellenburg, M P]]
-	[[Category: Ho, J X.]]	+	[[Category: Ho, J X]]
-	[[Category: Li, C.]]	+	[[Category: Li, C]]
-	[[Category: Ruble, J R.]]	+	[[Category: Ruble, J R]]
-	[[Category: Wang, Z M.]]	+	[[Category: Wang, Z M]]
	[[Category: Ferritin light chain perdeuterated]]		[[Category: Ferritin light chain perdeuterated]]
	[[Category: Metal binding protein]]		[[Category: Metal binding protein]]

OCA at 01:02, 30 September 2014

OCA — Tue, 30 Sep 2014 01:02:26 GMT

←Older revision		Revision as of 01:02, 30 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2fg8~~\| ~~PDB~~=2fg8 \| ~~SCENE~~= }}	+	==Structure of Human Ferritin L Chain==
-	===~~Structure~~ of ~~Human Ferritin L Chain~~===	+	<StructureSection load='2fg8' size='340' side='right' caption='[[2fg8]], [[Resolution\|resolution]] 2.50Å' scene=''>
-	~~{{ABSTRACT_PUBMED_16790936}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2fg8]] is a 8 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=2FG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2FG8 FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CS:CESIUM+ION'>CS</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fg4\|2fg4]], [[2ffx\|2ffx]]</td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">FTL ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=2fg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2fg8 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2fg8 RCSB], [http://www.ebi.ac.uk/pdbsum/2fg8 PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[http://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[http://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref> <ref>PMID:16116125</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref> <ref>PMID:20159981</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/fg/2fg8_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 ==
		+	Ferritin is the major iron-storage protein present in all cells. It generally contains 24 subunits, with different ratios of heavy chain (H) to light chain (L), in the shape of a hollow sphere hosting up to 4500 ferric Fe atoms inside. H-rich ferritins catalyse the oxidation of iron(II), while L-rich ferritins promote the nucleation and storage of iron(III). Several X-ray structures have been determined, including those of L-chain ferritins from horse spleen (HoSF), recombinant L-chain ferritins from horse (HoLF), mouse (MoLF) and bullfrog (BfLF) as well as recombinant human H-chain ferritin (HuHF). Here, structures have been determined of two crystal forms of recombinant human L-chain ferritin (HuLF) obtained from native and perdeuterated proteins. The structures show a cluster of acidic residues at the ferrihydrite nucleation site and at the iron channel along the threefold axis. An ordered Cd2+ structure is observed within the iron channel, offering further insight into the route and mechanism of iron transport into the capsid. The loop between helices D and E, which is disordered in many other L-chain structures, is clearly visible in these two structures. The crystals generated from perdeuterated HuLF will be used for neutron diffraction studies.

-	~~==Disease==~~	+	Structure of human ferritin L chain.,Wang Z, Li C, Ellenburg M, Soistman E, Ruble J, Wright B, Ho JX, Carter DC Acta Crystallogr D Biol Crystallogr. 2006 Jul;62(Pt 7):800-6. Epub 2006, Jun 20. PMID:16790936<ref>PMID:16790936</ref>
-	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[http://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of ~~circulating~~ ferritin. ~~HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene~~.~~<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3~~ (~~NBIA3~~) ~~[MIM~~:~~[http://omim.org/entry/606159 606159]]; also known as adult~~-~~onset basal ganglia disease~~. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, ~~mild nonprogressive cognitive deficit and episodic psychosis~~. ~~It is linked with decreased serum ferritin levels.<ref>~~PMID:~~20159981</ref>~~<ref>PMID:~~16116125~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble~~, ~~non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays~~ a ~~role in delivery~~ of ~~iron to cells~~. ~~Mediates iron uptake in capsule cells~~ of ~~the developing kidney (By similarity)~~.<~~ref~~>~~PMID:19923220~~</~~ref~~>~~<ref>PMID:20159981</ref>~~	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[2fg8]] is a 8 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=2FG8 OCA].	+

	==See Also==		==See Also==
	*[[Ferritin\|Ferritin]]		*[[Ferritin\|Ferritin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:016790936</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Carter, D C.]]		[[Category: Carter, D C.]]

OCA at 04:38, 25 March 2013

OCA — Mon, 25 Mar 2013 04:38:57 GMT

←Older revision		Revision as of 04:38, 25 March 2013
Line 1:		Line 1:
-	[[Image:2fg8.png\|left\|200px]]
-
	{{STRUCTURE_2fg8\| PDB=2fg8 \| SCENE= }}		{{STRUCTURE_2fg8\| PDB=2fg8 \| SCENE= }}
-
	===Structure of Human Ferritin L Chain===		===Structure of Human Ferritin L Chain===
		+	{{ABSTRACT_PUBMED_16790936}}

-	~~{{ABSTRACT_PUBMED_16790936}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Defects in FTL are the cause of hereditary hyperferritinemia-cataract syndrome (HHCS) [MIM:[http://omim.org/entry/600886 600886]]. It is an autosomal dominant disease characterized by early-onset bilateral cataract. Affected patients have elevated level of circulating ferritin. HHCS is caused by mutations in the iron responsive element (IRE) of the FTL gene.<ref>PMID:20159981</ref> Defects in FTL are the cause of neurodegeneration with brain iron accumulation type 3 (NBIA3) [MIM:[http://omim.org/entry/606159 606159]]; also known as adult-onset basal ganglia disease. It is a movement disorder with heterogeneous presentations starting in the fourth to sixth decade. It is characterized by a variety of neurological signs including parkinsonism, ataxia, corticospinal signs, mild nonprogressive cognitive deficit and episodic psychosis. It is linked with decreased serum ferritin levels.<ref>PMID:20159981</ref><ref>PMID:16116125</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/FRIL_HUMAN FRIL_HUMAN]] Stores iron in a soluble, non-toxic, readily available form. Important for iron homeostasis. Iron is taken up in the ferrous form and deposited as ferric hydroxides after oxidation. Also plays a role in delivery of iron to cells. Mediates iron uptake in capsule cells of the developing kidney (By similarity).<ref>PMID:19923220</ref><ref>PMID:20159981</ref>

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:016790936</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016790936</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Carter, D C.]]		[[Category: Carter, D C.]]

OCA at 17:29, 20 October 2012

OCA — Sat, 20 Oct 2012 17:29:23 GMT

←Older revision		Revision as of 17:29, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[2fg8]] is a 8 chain structure ~~of [[Ferritin]]~~ 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=2FG8 OCA].	+	[[2fg8]] is a 8 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=2FG8 OCA].

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

OCA at 01:03, 27 July 2012

OCA — Fri, 27 Jul 2012 01:03:19 GMT

←Older revision		Revision as of 01:03, 27 July 2012
Line 1:		Line 1:
	[[Image:2fg8.png\|left\|200px]]		[[Image:2fg8.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_2fg8", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_2fg8\| PDB=2fg8 \| SCENE= }}		{{STRUCTURE_2fg8\| PDB=2fg8 \| SCENE= }}

	===Structure of Human Ferritin L Chain===		===Structure of Human Ferritin L Chain===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_16790936}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 16790936 is the PubMed ID number.
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	{{ABSTRACT_PUBMED_16790936}}		{{ABSTRACT_PUBMED_16790936}}

Line 22:		Line 11:

	==See Also==		==See Also==
-	*[[Ferritin]]	+	*[[Ferritin\|Ferritin]]

	==Reference==		==Reference==

OCA at 10:30, 16 November 2011

OCA — Wed, 16 Nov 2011 10:30:44 GMT

←Older revision		Revision as of 10:30, 16 November 2011
Line 25:		Line 25:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~16790936~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016790936</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Carter, D C.]]		[[Category: Carter, D C.]]