2j5w
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2j5w]] 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=2J5W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2J5W FirstGlance]. <br> | <table><tr><td colspan='2'>[[2j5w]] 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=2J5W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2J5W FirstGlance]. <br> | ||
| - | </td></tr><tr><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CU:COPPER+(II)+ION'>CU</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=O:OXYGEN+ATOM'>O</scene>, <scene name='pdbligand=OXY:OXYGEN+MOLECULE'>OXY</scene>< | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=CU:COPPER+(II)+ION'>CU</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=O:OXYGEN+ATOM'>O</scene>, <scene name='pdbligand=OXY:OXYGEN+MOLECULE'>OXY</scene></td></tr> |
| - | <tr><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1kcw|1kcw]]</td></tr> | + | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1kcw|1kcw]]</td></tr> |
| - | <tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Ferroxidase Ferroxidase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=1.16.3.1 1.16.3.1] </span></td></tr> | + | <tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Ferroxidase Ferroxidase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=1.16.3.1 1.16.3.1] </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=2j5w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2j5w OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2j5w RCSB], [http://www.ebi.ac.uk/pdbsum/2j5w 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=2j5w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2j5w OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2j5w RCSB], [http://www.ebi.ac.uk/pdbsum/2j5w PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/CERU_HUMAN CERU_HUMAN]] Defects in CP are the cause of aceruloplasminemia (ACERULOP) [MIM:[http://omim.org/entry/604290 604290]]. It is an autosomal recessive disorder of iron metabolism characterized by iron accumulation in the brain as well as visceral organs. Clinical features consist of the triad of retinal degeneration, diabetes mellitus and neurological disturbances. Note=Ceruloplasmin levels are decreased in Wilson disease, in which copper cannot be incorporated into ceruloplasmin in liver because of defects in the copper-transporting ATPase 2. | [[http://www.uniprot.org/uniprot/CERU_HUMAN CERU_HUMAN]] Defects in CP are the cause of aceruloplasminemia (ACERULOP) [MIM:[http://omim.org/entry/604290 604290]]. It is an autosomal recessive disorder of iron metabolism characterized by iron accumulation in the brain as well as visceral organs. Clinical features consist of the triad of retinal degeneration, diabetes mellitus and neurological disturbances. Note=Ceruloplasmin levels are decreased in Wilson disease, in which copper cannot be incorporated into ceruloplasmin in liver because of defects in the copper-transporting ATPase 2. | ||
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[[Category: Ferroxidase]] | [[Category: Ferroxidase]] | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Bento, I | + | [[Category: Bento, I]] |
| - | [[Category: Lindley, P F | + | [[Category: Lindley, P F]] |
| - | [[Category: Peixoto, C | + | [[Category: Peixoto, C]] |
| - | [[Category: Zaitsev, V N | + | [[Category: Zaitsev, V N]] |
[[Category: Ceruloplasmin]] | [[Category: Ceruloplasmin]] | ||
[[Category: Copper transport]] | [[Category: Copper transport]] | ||
Revision as of 17:03, 19 January 2015
CERULOPLASMIN REVISITED: STRUCTURAL AND FUNCTIONAL ROLES OF VARIOUS METAL CATION BINDING SITES
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