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5lg8

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Current revision (08:59, 11 October 2023) (edit) (undo)
 
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==Human L-type ferritin iron loaded for 60 minutes==
==Human L-type ferritin iron loaded for 60 minutes==
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<StructureSection load='5lg8' size='340' side='right' caption='[[5lg8]], [[Resolution|resolution]] 1.98&Aring;' scene=''>
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<StructureSection load='5lg8' size='340' side='right'caption='[[5lg8]], [[Resolution|resolution]] 1.98&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[5lg8]] 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=5LG8 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5LG8 FirstGlance]. <br>
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<table><tr><td colspan='2'>[[5lg8]] 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=5LG8 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5LG8 FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=FE:FE+(III)+ION'>FE</scene>, <scene name='pdbligand=OXY:OXYGEN+MOLECULE'>OXY</scene>, <scene name='pdbligand=PER:PEROXIDE+ION'>PER</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.98&#8491;</td></tr>
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<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5lg2|5lg2]]</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CD:CADMIUM+ION'>CD</scene>, <scene name='pdbligand=FE:FE+(III)+ION'>FE</scene>, <scene name='pdbligand=OXY:OXYGEN+MOLECULE'>OXY</scene>, <scene name='pdbligand=PER:PEROXIDE+ION'>PER</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
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<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>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5lg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5lg8 OCA], [https://pdbe.org/5lg8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5lg8 RCSB], [https://www.ebi.ac.uk/pdbsum/5lg8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5lg8 ProSAT]</span></td></tr>
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<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=5lg8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5lg8 OCA], [http://pdbe.org/5lg8 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5lg8 RCSB], [http://www.ebi.ac.uk/pdbsum/5lg8 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5lg8 ProSAT]</span></td></tr>
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</table>
</table>
== Disease ==
== Disease ==
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[[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>
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[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 ==
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[[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>
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[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>
<div style="background-color:#fffaf0;">
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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</div>
</div>
<div class="pdbe-citations 5lg8" style="background-color:#fffaf0;"></div>
<div class="pdbe-citations 5lg8" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Ferritin 3D structures|Ferritin 3D structures]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
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[[Category: Human]]
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[[Category: Homo sapiens]]
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[[Category: Mangani, S]]
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[[Category: Large Structures]]
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[[Category: Pisa, F Di]]
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[[Category: Di Pisa F]]
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[[Category: Pozzi, C]]
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[[Category: Mangani S]]
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[[Category: Ferritin]]
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[[Category: Pozzi C]]
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[[Category: Iron]]
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[[Category: L-type]]
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[[Category: Metal binding protein]]
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[[Category: Mineralization]]
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Current revision

Human L-type ferritin iron loaded for 60 minutes

PDB ID 5lg8

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