1qrk: Difference between revisions

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<StructureSection load='1qrk' size='340' side='right'caption='[[1qrk]], [[Resolution|resolution]] 2.50&Aring;' scene=''>
<StructureSection load='1qrk' size='340' side='right'caption='[[1qrk]], [[Resolution|resolution]] 2.50&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[1qrk]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1bl2 1bl2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1QRK OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1QRK FirstGlance]. <br>
<table><tr><td colspan='2'>[[1qrk]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1bl2 1bl2]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1QRK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1QRK FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SR:STRONTIUM+ION'>SR</scene></td></tr>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SR:STRONTIUM+ION'>SR</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1ggt|1ggt]], [[1fie|1fie]], [[1ggu|1ggu]], [[1ggy|1ggy]]</td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1ggt|1ggt]], [[1fie|1fie]], [[1ggu|1ggu]], [[1ggy|1ggy]]</div></td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Protein-glutamine_gamma-glutamyltransferase Protein-glutamine gamma-glutamyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.2.13 2.3.2.13] </span></td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Protein-glutamine_gamma-glutamyltransferase Protein-glutamine gamma-glutamyltransferase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.2.13 2.3.2.13] </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=1qrk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1qrk OCA], [http://pdbe.org/1qrk PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1qrk RCSB], [http://www.ebi.ac.uk/pdbsum/1qrk PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1qrk 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=1qrk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1qrk OCA], [https://pdbe.org/1qrk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1qrk RCSB], [https://www.ebi.ac.uk/pdbsum/1qrk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1qrk ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Defects in F13A1 are the cause of factor XIII subunit A deficiency (FA13AD) [MIM:[http://omim.org/entry/613225 613225]]. FA13AD is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.<ref>PMID:1353995</ref>   
[[https://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Defects in F13A1 are the cause of factor XIII subunit A deficiency (FA13AD) [MIM:[https://omim.org/entry/613225 613225]]. FA13AD is an autosomal recessive disorder characterized by a life-long bleeding tendency, impaired wound healing and spontaneous abortion in affected women.<ref>PMID:1353995</ref>   
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Factor XIII is activated by thrombin and calcium ion to a transglutaminase that catalyzes the formation of gamma-glutamyl-epsilon-lysine cross-links between fibrin chains, thus stabilizing the fibrin clot. Also cross-link alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin.  
[[https://www.uniprot.org/uniprot/F13A_HUMAN F13A_HUMAN]] Factor XIII is activated by thrombin and calcium ion to a transglutaminase that catalyzes the formation of gamma-glutamyl-epsilon-lysine cross-links between fibrin chains, thus stabilizing the fibrin clot. Also cross-link alpha-2-plasmin inhibitor, or fibronectin, to the alpha chains of fibrin.  
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]

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