5tca: Difference between revisions
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<StructureSection load='5tca' size='340' side='right'caption='[[5tca]], [[Resolution|resolution]] 3.15Å' scene=''> | <StructureSection load='5tca' size='340' side='right'caption='[[5tca]], [[Resolution|resolution]] 3.15Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[5tca]] is a 7 chain structure with sequence from [ | <table><tr><td colspan='2'>[[5tca]] is a 7 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=5TCA OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5TCA FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.15Å</td></tr> | ||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=J55:1-(2-{(2S)-2-[(6-BROMOPYRIDIN-2-YL)CARBAMOYL]-1,3-THIAZOLIDIN-3-YL}-2-OXOETHYL)-1H-PYRAZOLO[3,4-B]PYRIDINE-3-CARBOXAMIDE'>J55</scene></td></tr> | |||
<tr id=' | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5tca FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tca OCA], [https://pdbe.org/5tca PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5tca RCSB], [https://www.ebi.ac.uk/pdbsum/5tca PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5tca ProSAT]</span></td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | |||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [https://www.uniprot.org/uniprot/CFAD_HUMAN CFAD_HUMAN] Defects in CFD are the cause of complement factor D deficiency (CFDD) [MIM:[https://omim.org/entry/613912 613912]. CFDD is an immunologic disorder characterized by increased susceptibility to bacterial infections, particularly Neisseria infections, due to a defect in the alternative complement pathway. | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/CFAD_HUMAN CFAD_HUMAN] Factor D cleaves factor B when the latter is complexed with factor C3b, activating the C3bbb complex, which then becomes the C3 convertase of the alternate pathway. Its function is homologous to that of C1s in the classical pathway. | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Stuckey | [[Category: Stuckey JA]] | ||