2win

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{{Large structure}}
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==C3 convertase (C3bBb) stabilized by SCIN==
==C3 convertase (C3bBb) stabilized by SCIN==
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<StructureSection load='2win' size='340' side='right' caption='[[2win]], [[Resolution|resolution]] 3.90&Aring;' scene=''>
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<StructureSection load='2win' size='340' side='right'caption='[[2win]], [[Resolution|resolution]] 3.90&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2win]] is a 16 chain structure with sequence from [http://en.wikipedia.org/wiki/"micrococcus_aureus"_(rosenbach_1884)_zopf_1885 "micrococcus aureus" (rosenbach 1884) zopf 1885], [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WIN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2WIN FirstGlance]. <br>
<table><tr><td colspan='2'>[[2win]] is a 16 chain structure with sequence from [http://en.wikipedia.org/wiki/"micrococcus_aureus"_(rosenbach_1884)_zopf_1885 "micrococcus aureus" (rosenbach 1884) zopf 1885], [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WIN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2WIN FirstGlance]. <br>
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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=2win FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2win OCA], [http://pdbe.org/2win PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2win RCSB], [http://www.ebi.ac.uk/pdbsum/2win PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2win ProSAT]</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=2win FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2win OCA], [http://pdbe.org/2win PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2win RCSB], [http://www.ebi.ac.uk/pdbsum/2win PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2win ProSAT]</span></td></tr>
</table>
</table>
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{{Large structure}}
 
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] Defects in C3 are the cause of complement component 3 deficiency (C3D) [MIM:[http://omim.org/entry/613779 613779]]. A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis.<ref>PMID:19913840</ref> <ref>PMID:9596584</ref> <ref>PMID:11387479</ref> <ref>PMID:15713468</ref> <ref>PMID:7961791</ref> [:] Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9) [MIM:[http://omim.org/entry/611378 611378]]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.<ref>PMID:19913840</ref> <ref>PMID:17634448</ref> Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5) [MIM:[http://omim.org/entry/612925 612925]]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.<ref>PMID:19913840</ref> <ref>PMID:18796626</ref> <ref>PMID:20513133</ref> Note=Increased levels of C3 and its cleavage product ASP, are associated with obesity, diabetes and coronary heart disease. Short-term endurance training reduces baseline ASP levels and subsequently fat storage.<ref>PMID:19913840</ref> [[http://www.uniprot.org/uniprot/CFAB_HUMAN CFAB_HUMAN]] Defects in CFB are a cause of susceptibility to hemolytic uremic syndrome atypical type 4 (AHUS4) [MIM:[http://omim.org/entry/612924 612924]]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.<ref>PMID:17182750</ref> <ref>PMID:20513133</ref>
[[http://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] Defects in C3 are the cause of complement component 3 deficiency (C3D) [MIM:[http://omim.org/entry/613779 613779]]. A rare defect of the complement classical pathway. Patients develop recurrent, severe, pyogenic infections because of ineffective opsonization of pathogens. Some patients may also develop autoimmune disorders, such as arthralgia and vasculitic rashes, lupus-like syndrome and membranoproliferative glomerulonephritis.<ref>PMID:19913840</ref> <ref>PMID:9596584</ref> <ref>PMID:11387479</ref> <ref>PMID:15713468</ref> <ref>PMID:7961791</ref> [:] Genetic variation in C3 is associated with susceptibility to age-related macular degeneration type 9 (ARMD9) [MIM:[http://omim.org/entry/611378 611378]]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.<ref>PMID:19913840</ref> <ref>PMID:17634448</ref> Defects in C3 are a cause of susceptibility to hemolytic uremic syndrome atypical type 5 (AHUS5) [MIM:[http://omim.org/entry/612925 612925]]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.<ref>PMID:19913840</ref> <ref>PMID:18796626</ref> <ref>PMID:20513133</ref> Note=Increased levels of C3 and its cleavage product ASP, are associated with obesity, diabetes and coronary heart disease. Short-term endurance training reduces baseline ASP levels and subsequently fat storage.<ref>PMID:19913840</ref> [[http://www.uniprot.org/uniprot/CFAB_HUMAN CFAB_HUMAN]] Defects in CFB are a cause of susceptibility to hemolytic uremic syndrome atypical type 4 (AHUS4) [MIM:[http://omim.org/entry/612924 612924]]. An atypical form of hemolytic uremic syndrome. It is a complex genetic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, renal failure and absence of episodes of enterocolitis and diarrhea. In contrast to typical hemolytic uremic syndrome, atypical forms have a poorer prognosis, with higher death rates and frequent progression to end-stage renal disease. Note=Susceptibility to the development of atypical hemolytic uremic syndrome can be conferred by mutations in various components of or regulatory factors in the complement cascade system. Other genes may play a role in modifying the phenotype.<ref>PMID:17182750</ref> <ref>PMID:20513133</ref>
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</div>
</div>
<div class="pdbe-citations 2win" style="background-color:#fffaf0;"></div>
<div class="pdbe-citations 2win" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Complement C3 3D structures|Complement C3 3D structures]]
== References ==
== References ==
<references/>
<references/>
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Human]]
[[Category: Human]]
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[[Category: Large Structures]]
[[Category: Gros, P]]
[[Category: Gros, P]]
[[Category: Janssen, B J]]
[[Category: Janssen, B J]]

Revision as of 13:45, 18 December 2019

C3 convertase (C3bBb) stabilized by SCIN

PDB ID 2win

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