6m3b: Difference between revisions

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OCA

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 <StructureSection load='6m3b' size='340' side='right'caption='[[6m3b]], [[Resolution|resolution]] 2.20&Aring;' scene=''>
 == Structural highlights ==
-<table><tr><td colspan='2'>[[6m3b]] is a 4 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=6M3B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6M3B FirstGlance]. <br>
+<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6M3B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6M3B FirstGlance]. <br>
 </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.2&#8491;</td></tr>
 <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></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=6m3b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6m3b OCA], [https://pdbe.org/6m3b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6m3b RCSB], [https://www.ebi.ac.uk/pdbsum/6m3b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6m3b ProSAT]</span></td></tr>
 </table>
-== Disease ==
-[https://www.uniprot.org/uniprot/PROC_HUMAN PROC_HUMAN] Defects in PROC are the cause of thrombophilia due to protein C deficiency, autosomal dominant (THPH3) [MIM:[https://omim.org/entry/176860 176860]. A hemostatic disorder characterized by impaired regulation of blood coagulation and a tendency to recurrent venous thrombosis. However, many adults with heterozygous disease may be asymptomatic. Individuals with decreased amounts of protein C are classically referred to as having type I protein C deficiency and those with normal amounts of a functionally defective protein as having type II deficiency.<ref>PMID:8560401</ref> <ref>PMID:2437584</ref> <ref>PMID:2602169</ref> <ref>PMID:1868249</ref> <ref>PMID:1347706</ref> <ref>PMID:1511989</ref> <ref>PMID:1301959</ref> <ref>PMID:8499568</ref> <ref>PMID:8292730</ref> <ref>PMID:8398832</ref> <ref>PMID:7865674</ref> <ref>PMID:7792728</ref> <ref>PMID:8829639</ref> <ref>PMID:9798967</ref>   Defects in PROC are the cause of thrombophilia due to protein C deficiency, autosomal recessive (THPH4) [MIM:[https://omim.org/entry/612304 612304]. A hemostatic disorder characterized by impaired regulation of blood coagulation and a tendency to recurrent venous thrombosis. It results in a thrombotic condition that can manifest as a severe neonatal disorder or as a milder disorder with late-onset thrombophilia. The severe form leads to neonatal death through massive neonatal venous thrombosis. Often associated with ecchymotic skin lesions which can turn necrotic called purpura fulminans, this disorder is very rare.
-== Function ==
-[https://www.uniprot.org/uniprot/PROC_HUMAN PROC_HUMAN] Protein C is a vitamin K-dependent serine protease that regulates blood coagulation by inactivating factors Va and VIIIa in the presence of calcium ions and phospholipids.
 <div style="background-color:#fffaf0;">
 == Publication Abstract from PubMed ==
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 __TOC__
 </StructureSection>
-[[Category: Homo sapiens]]
 [[Category: Large Structures]]
 [[Category: Egner U]]