2oay

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==Crystal structure of latent human C1-inhibitor==
==Crystal structure of latent human C1-inhibitor==
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<StructureSection load='2oay' size='340' side='right' caption='[[2oay]], [[Resolution|resolution]] 2.35&Aring;' scene=''>
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<StructureSection load='2oay' size='340' side='right'caption='[[2oay]], [[Resolution|resolution]] 2.35&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[2oay]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2OAY OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2OAY FirstGlance]. <br>
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<table><tr><td colspan='2'>[[2oay]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2OAY OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2OAY FirstGlance]. <br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">SERPING1, C1IN, C1NH ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">SERPING1, C1IN, C1NH ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
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<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=2oay FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2oay OCA], [http://pdbe.org/2oay PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2oay RCSB], [http://www.ebi.ac.uk/pdbsum/2oay PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2oay ProSAT]</span></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2oay FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2oay OCA], [https://pdbe.org/2oay PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2oay RCSB], [https://www.ebi.ac.uk/pdbsum/2oay PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2oay ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
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[[http://www.uniprot.org/uniprot/IC1_HUMAN IC1_HUMAN]] Defects in SERPING1 are the cause of hereditary angioedema (HAE) [MIM:[http://omim.org/entry/106100 106100]]; also called hereditary angioneurotic edema (HANE). HAE is an autosomal dominant disorder characterized by episodic local subcutaneous edema and submucosal edema involving the upper respiratory and gastrointestinal tracts. HAE due to C1 esterase inhibitor deficiency is comprised of two clinically indistinguishable forms. In HAE type 1, representing 85% of patients, serum levels of C1 esterase inhibitor are less than 35% of normal. In HAE type 2, the levels are normal or elevated, but the protein is non-functional.<ref>PMID:12773530</ref> <ref>PMID:7814636</ref> <ref>PMID:3178731</ref> <ref>PMID:2365061</ref> <ref>PMID:2296585</ref> <ref>PMID:2118657</ref> [:]<ref>PMID:1451784</ref> <ref>PMID:1363816</ref> <ref>PMID:8172583</ref> <ref>PMID:7883978</ref> <ref>PMID:8529136</ref> <ref>PMID:8755917</ref> <ref>PMID:14635117</ref> <ref>PMID:16409206</ref> <ref>PMID:22994404</ref>
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[[https://www.uniprot.org/uniprot/IC1_HUMAN IC1_HUMAN]] Defects in SERPING1 are the cause of hereditary angioedema (HAE) [MIM:[https://omim.org/entry/106100 106100]]; also called hereditary angioneurotic edema (HANE). HAE is an autosomal dominant disorder characterized by episodic local subcutaneous edema and submucosal edema involving the upper respiratory and gastrointestinal tracts. HAE due to C1 esterase inhibitor deficiency is comprised of two clinically indistinguishable forms. In HAE type 1, representing 85% of patients, serum levels of C1 esterase inhibitor are less than 35% of normal. In HAE type 2, the levels are normal or elevated, but the protein is non-functional.<ref>PMID:12773530</ref> <ref>PMID:7814636</ref> <ref>PMID:3178731</ref> <ref>PMID:2365061</ref> <ref>PMID:2296585</ref> <ref>PMID:2118657</ref> [:]<ref>PMID:1451784</ref> <ref>PMID:1363816</ref> <ref>PMID:8172583</ref> <ref>PMID:7883978</ref> <ref>PMID:8529136</ref> <ref>PMID:8755917</ref> <ref>PMID:14635117</ref> <ref>PMID:16409206</ref> <ref>PMID:22994404</ref>
== Function ==
== Function ==
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[[http://www.uniprot.org/uniprot/IC1_HUMAN IC1_HUMAN]] Activation of the C1 complex is under control of the C1-inhibitor. It forms a proteolytically inactive stoichiometric complex with the C1r or C1s proteases. May play a potentially crucial role in regulating important physiological pathways including complement activation, blood coagulation, fibrinolysis and the generation of kinins. Very efficient inhibitor of FXIIa. Inhibits chymotrypsin and kallikrein.<ref>PMID:8495195</ref>
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[[https://www.uniprot.org/uniprot/IC1_HUMAN IC1_HUMAN]] Activation of the C1 complex is under control of the C1-inhibitor. It forms a proteolytically inactive stoichiometric complex with the C1r or C1s proteases. May play a potentially crucial role in regulating important physiological pathways including complement activation, blood coagulation, fibrinolysis and the generation of kinins. Very efficient inhibitor of FXIIa. Inhibits chymotrypsin and kallikrein.<ref>PMID:8495195</ref>
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
Check<jmol>
<jmolCheckbox>
<jmolCheckbox>
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<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/oa/2oay_consurf.spt"</scriptWhenChecked>
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<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/oa/2oay_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
<text>to colour the structure by Evolutionary Conservation</text>
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</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Human]]
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[[Category: Large Structures]]
[[Category: Beinrohr, L]]
[[Category: Beinrohr, L]]
[[Category: Dobo, J]]
[[Category: Dobo, J]]

Revision as of 12:51, 9 June 2021

Crystal structure of latent human C1-inhibitor

PDB ID 2oay

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