1uor
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[1uor]] 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=1UOR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1UOR FirstGlance]. <br> | <table><tr><td colspan='2'>[[1uor]] 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=1UOR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1UOR FirstGlance]. <br> | ||
| - | </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=1uor FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uor OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1uor RCSB], [http://www.ebi.ac.uk/pdbsum/1uor PDBsum]</span></td></tr> | + | </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=1uor FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1uor OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1uor RCSB], [http://www.ebi.ac.uk/pdbsum/1uor PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/ALBU_HUMAN ALBU_HUMAN]] Defects in ALB are a cause of familial dysalbuminemic hyperthyroxinemia (FDH) [MIM:[http://omim.org/entry/103600 103600]]. FDH is a form of euthyroid hyperthyroxinemia that is due to increased affinity of ALB for T(4). It is the most common cause of inherited euthyroid hyperthyroxinemia in Caucasian population.<ref>PMID:8048949</ref> <ref>PMID:7852505</ref> <ref>PMID:9329347</ref> <ref>PMID:9589637</ref> | [[http://www.uniprot.org/uniprot/ALBU_HUMAN ALBU_HUMAN]] Defects in ALB are a cause of familial dysalbuminemic hyperthyroxinemia (FDH) [MIM:[http://omim.org/entry/103600 103600]]. FDH is a form of euthyroid hyperthyroxinemia that is due to increased affinity of ALB for T(4). It is the most common cause of inherited euthyroid hyperthyroxinemia in Caucasian population.<ref>PMID:8048949</ref> <ref>PMID:7852505</ref> <ref>PMID:9329347</ref> <ref>PMID:9589637</ref> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: Carter, D C | + | [[Category: Carter, D C]] |
| - | [[Category: Ho, J X | + | [[Category: Ho, J X]] |
[[Category: Metal-binding protein]] | [[Category: Metal-binding protein]] | ||
[[Category: Plasma protein]] | [[Category: Plasma protein]] | ||
Revision as of 13:00, 6 January 2015
X-RAY STUDY OF RECOMBINANT HUMAN SERUM ALBUMIN. PHASES DETERMINED BY MOLECULAR REPLACEMENT METHOD, USING LOW RESOLUTION STRUCTURE MODEL OF TETRAGONAL FORM OF HUMAN SERUM ALBUMIN
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