Complement C3: Difference between revisions

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<StructureSection load='2icf' size='340' side='right' caption='Structure of human glycosylated complement C3b α (grey) and β (green) chains complex with protein CRIG (khaki) and Ca+2 ion (green) (PDB code [[2icf]]).' scene=''>
<StructureSection load='2icf' size='340' side='right' caption='Structure of human glycosylated complement C3b α (magenta) and β (salmon) chains complex with protein CRIG (cyan) and Ca+2 ion (green) (PDB code [[2icf]]).' scene='59/594590/Cv/1'>
__TOC__
== Function ==


== Function ==
'''Complement C3''' (CC3) activates the complement system which is part of the immune response.  '''CC3''' is proteolytically cleaved by C3 convertase to '''C3a''' (residues 672-748) and '''C3b''' (residues 23-667, 749-1663). 
*'''C3a''' is a mediator of local inflammatory processes. 
*'''C3b''' binds covalently to cell surface carbohydrates or immune aggregates. 
*'''C3c''' is another C3b cleavage product residues: 23-664, 749-954, 1321-1663.<ref>PMID:11414361</ref>
*'''C3d''' is a fragment generated by C3b(residues 996-1287) which binds to antigens enhancing their uptake by B cells<ref>PMID:17337780</ref>.
 
<scene name='59/594590/Cv/2'>C3b α and β chains with protein CRIG and Ca+2 ion</scene>.


'''Complement C3''' (CC3) activates the complement system which is part of the immune response. CC3 is proteolytically cleaved by C3 convertase to C3a (residues 672-748) and C3b (residues 23-667, 749-1663).  C3a is a mediator of local inflammatory processes.  C3b binds covalently to cell surface carbohydrates or immune aggregates.  Breakdown of C3b generates the fragment C3d (residues 996-1287) which binds to antigens enhancing their uptake by B cells.  C3c is another C3b cleavage product residues: 23-664, 749-954, 1321-1663.
<scene name='59/594590/Cv/4'>Ca+2 ion coordination site</scene> (PDB code [[2icf]]).<ref>PMID:17051150</ref>


== Disease ==
== Disease ==
A mutation in CC3 cause the progressive kidney disease: dense deposit disease.  Other mutations are associated with recurrent bacterial infections.


== Relevance ==
== Relevance ==


== Structural highlights ==
Low levels of CC3 in the blood are associated with some kidney diseases.


==3D structures of complement C3==
==3D structures of complement C3==
[[Complement C3 3D structures]]


Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
</StructureSection>
 
===CC3===
 
[[2a73]] – hCC3 – human <br />
[[2b39]] – bCC3 – bovine <br />
 
===CC3a (anaphylatoxin)===
 
[[4hw5]], [[4hwj]], [[4i6o]] – hCC3  <br />
 
===CC3b===
 
[[2hr0]], [[2i07]] – hCC3  β+α’ chains<br />
[[2icf]] – hCC3 α+β chains + protein CRIG<br />
[[3g6j]] – hCC3 α+β chains + antibody<br />
[[2xwb]] – hCC3 α+β chains + complement factor B + complement factor D<br />
[[2xwj]] – hCC3 α+β chains (mutant) + complement factor B<br />
[[2wii]] – hCC3 α+β chains + complement factor H 1-4 sushi domains<br />
[[3l5n]], [[3ohx]] – hCC3 α+β chains + staphylococcal complement inhibitor<br />
[[2win]] – hCC3 α+β chains + complement factor B BB fragment + staphylococcal complement inhibitor<br />
 
===CC3c===
 
[[2a74]] – hCC3  <br />
[[2qki]] – hCC3 + compstatin <br />
[[3l3o]], [[3nms]] – hCC3 + staphylococcal complement inhibitor<br />
[[2ice]] – hCC3 α+β chains + protein CRIG<br />
[[3t4a]] – hCC3 α+β chains + fibrinogen-binding protein <br />
 
===CC3d===
 
[[1c3d]] – hCC3 (mutant) <br />
[[1w2s]], [[3oed]] – hCC3 1-2 sushi domains + complement receptor type 2 precursor<br />
[[2gox]], [[3d5r]], [[3d5s]] – hCC3 α chain fragment + fibrinogen-binding protein <br />
[[2noj]] – hCC3 α chain fragment (mutant) + EFB homologous protein <br />
[[2wy7]], [[2wy8]] – hCC3 α chain fragment (mutant) + IGG-binding protein <br />
[[3oxu]] – hCC3 α chain fragment (mutant) + HF protein <br />
[[4m76]] – hCC3 α chain fragment (mutant) + integrin α-M <br />
[[2xqw]] – hCC3  + complement factor H 19-20 sushi domains<br />
[[3rj3]] – hCC3 α chain fragment + complement factor H-related protein<br />
[[1qqf]] – rCC3 G fragment - rat <br />
[[1qsj]] – rCC3 G fragment (mutant) <br />
 
 
 
 
 


== References ==
== References ==

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Michal Harel, Alexander Berchansky