9zcj: Difference between revisions

Line 1:

~~'''Unreleased structure'''~~

~~The entry~~ 9zcj is ~~ON HOLD until Paper Publication~~

==Therapeutic antibody with captured antigen==

~~Authors~~: ~~Gorman~~, M.A., ~~Parker~~, M.W.

== Structural highlights ==

<table><tr><td colspan='2'>[[9zcj]] 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=9ZCJ OCA]. For a guided tour on the structure components use [https://proteopedia.org/fgij/fg.htm?mol=9ZCJ FirstGlance].

~~Description~~: ~~Therapeutic antibody~~ with ~~captured antigen~~

</td></tr><tr id='method'><td class="sblockLbl">[[Empirical_models|Method:]]</td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.6Å</td></tr>

[[Category: ~~Unreleased~~ Structures]]

<tr id='ligand'><td class="sblockLbl">[[Ligand|Ligands:]]</td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>

[[Category: Gorman~~, M.A~~]]

<tr id='resources'><td class="sblockLbl">Resources:</td><td class="sblockDat">[https://proteopedia.org/fgij/fg.htm?mol=9zcj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9zcj OCA], [https://pdbe.org/9zcj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9zcj RCSB], [https://www.ebi.ac.uk/pdbsum/9zcj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9zcj ProSAT]</td></tr>

[[Category: Parker~~, M.W~~]]

</table>

== Disease ==

[https://www.uniprot.org/uniprot/CO2_HUMAN CO2_HUMAN] Defects in C2 are the cause of complement component 2 deficiency (C2D) [MIM:[https://omim.org/entry/217000 217000]. A deficiency of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus erythematosus. Skin and joint manifestations are common and renal disease is relatively rare. Patients with complement component 2 deficiency are also reported to have recurrent or invasive infections.<ref>PMID:8621452</ref> <ref>PMID:9670930</ref>

== Function ==

[https://www.uniprot.org/uniprot/CO2_HUMAN CO2_HUMAN] Component C2 which is part of the classical pathway of the complement system is cleaved by activated factor C1 into two fragments: C2b and C2a. C2a, a serine protease, then combines with complement factor 4b to generate the C3 or C5 convertase.

== References ==

__TOC__

</StructureSection>

[[Category: Homo sapiens]]

[[Category: Large Structures]]

[[Category: Gorman MA]]

[[Category: Parker MW]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 9zcj is ON HOLD  until Paper Publication
+==Therapeutic antibody with captured antigen==
+<StructureSection load='9zcj' size='340' side='right'caption='[[9zcj]], [[Resolution|resolution]] 2.60&Aring;' scene=''>
-Authors: Gorman, M.A., Parker, M.W.
+== Structural highlights ==
+<table><tr><td colspan='2'>[[9zcj]] 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=9ZCJ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9ZCJ FirstGlance]. <br>
-Description: Therapeutic antibody with captured antigen
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.6&#8491;</td></tr>
-[[Category: Unreleased Structures]]
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
-[[Category: Gorman, M.A]]
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9zcj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9zcj OCA], [https://pdbe.org/9zcj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9zcj RCSB], [https://www.ebi.ac.uk/pdbsum/9zcj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9zcj ProSAT]</span></td></tr>
-[[Category: Parker, M.W]]
+</table>
+== Disease ==
+[https://www.uniprot.org/uniprot/CO2_HUMAN CO2_HUMAN] Defects in C2 are the cause of complement component 2 deficiency (C2D) [MIM:[https://omim.org/entry/217000 217000]. A deficiency of the complement classical pathway associated with the development of autoimmune disorders, mainly systemic lupus erythematosus. Skin and joint manifestations are common and renal disease is relatively rare. Patients with complement component 2 deficiency are also reported to have recurrent or invasive infections.<ref>PMID:8621452</ref> <ref>PMID:9670930</ref>
+== Function ==
+[https://www.uniprot.org/uniprot/CO2_HUMAN CO2_HUMAN] Component C2 which is part of the classical pathway of the complement system is cleaved by activated factor C1 into two fragments: C2b and C2a. C2a, a serine protease, then combines with complement factor 4b to generate the C3 or C5 convertase.
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Homo sapiens]]
+[[Category: Large Structures]]
+[[Category: Gorman MA]]
+[[Category: Parker MW]]