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4d9r
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| - | {{STRUCTURE_4d9r| PDB=4d9r | SCENE= }} | ||
| - | ===Inhibiting Alternative Pathway Complement Activation by Targeting the Exosite on Factor D=== | ||
| - | {{ABSTRACT_PUBMED_22362762}} | ||
| - | == | + | ==Inhibiting Alternative Pathway Complement Activation by Targeting the Exosite on Factor D== |
| - | [[http://www.uniprot.org/uniprot/CFAD_HUMAN CFAD_HUMAN | + | <StructureSection load='4d9r' size='340' side='right'caption='[[4d9r]], [[Resolution|resolution]] 2.42Å' scene=''> |
| + | == Structural highlights == | ||
| + | <table><tr><td colspan='2'>[[4d9r]] is a 6 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=4D9R OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4D9R 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]] 2.42Å</td></tr> | ||
| + | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</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=4d9r FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4d9r OCA], [https://pdbe.org/4d9r PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4d9r RCSB], [https://www.ebi.ac.uk/pdbsum/4d9r PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4d9r ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == 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 == | ||
| + | [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. | ||
| - | == | + | ==See Also== |
| - | [[ | + | *[[Complement factor 3D structures|Complement factor 3D structures]] |
| - | + | __TOC__ | |
| - | + | </StructureSection> | |
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[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
| - | [[Category: | + | [[Category: Large Structures]] |
| - | [[Category: | + | [[Category: Murray JM]] |
| - | [[Category: | + | [[Category: Wiesmann C]] |
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Current revision
Inhibiting Alternative Pathway Complement Activation by Targeting the Exosite on Factor D
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