4hwj - Revision history

OCA at 08:20, 9 November 2022

OCA — Wed, 09 Nov 2022 08:20:05 GMT

←Older revision		Revision as of 08:20, 9 November 2022
Line 1:		Line 1:

	==Crystal Structure of the Human C3a desArg anaphylatoxin==		==Crystal Structure of the Human C3a desArg anaphylatoxin==
-	<StructureSection load='4hwj' size='340' side='right' caption='[[4hwj]], [[Resolution\|resolution]] 2.60Å' scene=''>	+	<StructureSection load='4hwj' size='340' side='right'caption='[[4hwj]], [[Resolution\|resolution]] 2.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4hwj]] 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=4HWJ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4HWJ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4hwj]] is a 1 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=4HWJ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4HWJ FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4hw5\|4hw5]]</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=4hwj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4hwj OCA], [https://pdbe.org/4hwj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4hwj RCSB], [https://www.ebi.ac.uk/pdbsum/4hwj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4hwj ProSAT]</span></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">C3, CPAMD1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</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=4hwj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4hwj OCA], [~~http~~://pdbe.org/4hwj PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=4hwj RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/4hwj PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=4hwj ProSAT]</span></td></tr>	+
	</table>		</table>
	== 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>	+	[https://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN] Defects in C3 are the cause of complement component 3 deficiency (C3D) [MIM:[https://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:[https://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:[https://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>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref>	+	[https://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN] C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 24:		Line 22:

	==See Also==		==See Also==
-	*[[Complement C3\|Complement C3]]	+	*[[Complement C3 3D structures\|Complement C3 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Andersen, G R~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Bajic, G~~]]	+	[[Category: Andersen GR]]
-	[[Category: ~~Yatime, L~~]]	+	[[Category: Bajic G]]
-	[[Category: ~~Anaphylatoxin]]~~	+	[[Category: Yatime L]]
-	~~[[Category: C3a]]~~	+
-	~~[[Category: C3a desarg]]~~	+
-	~~[[Category: C5a]]~~	+
-	~~[[Category: C5a desarg]]~~	+
-	~~[[Category: Complement system]]~~	+
-	~~[[Category: Four-helix-bundle]]~~	+
-	~~[[Category: Immune system]]~~	+
-	~~[[Category: Inflammation]]~~	+
-	~~[[Category: Innate immunity~~]]	+

OCA at 09:19, 11 August 2016

OCA — Thu, 11 Aug 2016 09:19:15 GMT

←Older revision		Revision as of 09:19, 11 August 2016
Line 1:		Line 1:
		+
	==Crystal Structure of the Human C3a desArg anaphylatoxin==		==Crystal Structure of the Human C3a desArg anaphylatoxin==
	<StructureSection load='4hwj' size='340' side='right' caption='[[4hwj]], [[Resolution\|resolution]] 2.60Å' scene=''>		<StructureSection load='4hwj' size='340' side='right' caption='[[4hwj]], [[Resolution\|resolution]] 2.60Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4hwj]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4HWJ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4hwj]] 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=4HWJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4HWJ FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4hw5\|4hw5]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4hw5\|4hw5]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">C3, CPAMD1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">C3, CPAMD1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=4hwj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4hwj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4hwj RCSB], [http://www.ebi.ac.uk/pdbsum/4hwj PDBsum]</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=4hwj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4hwj OCA], [http://pdbe.org/4hwj PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4hwj RCSB], [http://www.ebi.ac.uk/pdbsum/4hwj PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4hwj ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 4hwj" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 27:		Line 29:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Andersen, G R]]		[[Category: Andersen, G R]]
	[[Category: Bajic, G]]		[[Category: Bajic, G]]

OCA at 10:24, 25 January 2015

OCA — Sun, 25 Jan 2015 10:24:26 GMT

←Older revision		Revision as of 10:24, 25 January 2015
Line 1:		Line 1:
-	~~{{STRUCTURE_4hwj~~\| ~~PDB~~=4hwj \| ~~SCENE~~= }}	+	==Crystal Structure of the Human C3a desArg anaphylatoxin==
-	===~~Crystal Structure~~ of the ~~Human~~ C3a ~~desArg~~ anaphylatoxin===	+	<StructureSection load='4hwj' size='340' side='right' caption='[[4hwj]], [[Resolution\|resolution]] 2.60Å' scene=''>
-	~~{{ABSTRACT_PUBMED_23184394}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[4hwj]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4HWJ FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[4hw5\|4hw5]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">C3, CPAMD1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=4hwj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4hwj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4hwj RCSB], [http://www.ebi.ac.uk/pdbsum/4hwj PDBsum]</span></td></tr>
		+	</table>
		+	== 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>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref> Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77.<ref>PMID:8376604</ref> <ref>PMID:2909530</ref> <ref>PMID:9059512</ref> <ref>PMID:9555951</ref> <ref>PMID:10432298</ref> <ref>PMID:15833747</ref> <ref>PMID:16333141</ref> <ref>PMID:19615750</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Complement is a part of innate immunity that has a critical role in the protection against microbial infections, bridges the innate with the adaptive immunity and initiates inflammation. Activation of the complement, by specific recognition of molecular patterns presented by an activator, e.g. a pathogen cell, in the classical and lectin pathways or spontaneously in the alternative pathway, leads to the opsonization of the activator and the production of pro-inflammatory molecules such as the C3a anaphylatoxin. The biological function of this anaphylatoxin is regulated by carboxypeptidase B, a plasma protease that cleaves off the C-terminal arginine yielding C3a desArg, an inactive form. While functional assays demonstrate strikingly different physiological effects between C3a and C3a desArg, no structural information is available on the possible conformational differences between the two proteins. Here, we report a novel and simple expression and purification protocol for recombinant human C3a and C3a desArg anaphylatoxins, as well as their crystal structures at 2.3 and 2.6 A respectively. Structural analysis revealed no significant conformational differences between the two anaphylatoxins in contrast to what has been reported for C5a and C5a desArg. We compare the structures of different anaphylatoxins and discuss the relevance of their observed conformations to complement activation and binding of the anaphylatoxins to their cognate receptors.

-	~~==Disease==~~	+	Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg.,Bajic G, Yatime L, Klos A, Andersen GR Protein Sci. 2012 Nov 26. doi: 10.1002/pro.2200. PMID:23184394<ref>PMID:23184394</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>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~//www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.<ref>PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750</ref> Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a ~~mediator~~ of ~~local inflammatory process. It induces~~ the ~~contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes~~.<ref>PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750</ref> Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. ~~Appears to stimulate TG synthesis via activation~~ of ~~the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77~~.<~~ref~~>~~PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750~~</~~ref~~>	+	</div>

-	==~~About this Structure~~==	+	==See Also==
-	[[~~4hwj~~]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA].	+	*[[Complement C3\|Complement C3]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Andersen, G R.]]	+	[[Category: Andersen, G R]]
-	[[Category: Bajic, G.]]	+	[[Category: Bajic, G]]
-	[[Category: Yatime, L.]]	+	[[Category: Yatime, L]]
	[[Category: Anaphylatoxin]]		[[Category: Anaphylatoxin]]
	[[Category: C3a]]		[[Category: C3a]]

OCA at 16:12, 24 March 2013

OCA — Sun, 24 Mar 2013 16:12:20 GMT

←Older revision		Revision as of 16:12, 24 March 2013
Line 1:		Line 1:
-	[[Image:4hwj.png\|left\|200px]]
-
	{{STRUCTURE_4hwj\| PDB=4hwj \| SCENE= }}		{{STRUCTURE_4hwj\| PDB=4hwj \| SCENE= }}
-
	===Crystal Structure of the Human C3a desArg anaphylatoxin===		===Crystal Structure of the Human C3a desArg anaphylatoxin===
-
	{{ABSTRACT_PUBMED_23184394}}		{{ABSTRACT_PUBMED_23184394}}
		+
		+	==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>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/CO3_HUMAN CO3_HUMAN]] C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.<ref>PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750</ref> Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes.<ref>PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750</ref> Acylation stimulating protein (ASP): adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for GPR77. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of GPR77.<ref>PMID:8376604</ref><ref>PMID:2909530</ref><ref>PMID:9059512</ref><ref>PMID:9555951</ref><ref>PMID:10432298</ref><ref>PMID:15833747</ref><ref>PMID:16333141</ref><ref>PMID:19615750</ref>

	==About this Structure==		==About this Structure==
	[[4hwj]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA].		[[4hwj]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA].
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Andersen, G R.]]		[[Category: Andersen, G R.]]

OCA at 09:41, 13 February 2013

OCA — Wed, 13 Feb 2013 09:41:07 GMT

←Older revision		Revision as of 09:41, 13 February 2013
Line 1:		Line 1:
-	[[Image:4hwj.~~jpg~~\|left\|200px]]	+	[[Image:4hwj.png\|left\|200px]]

	{{STRUCTURE_4hwj\| PDB=4hwj \| SCENE= }}		{{STRUCTURE_4hwj\| PDB=4hwj \| SCENE= }}

OCA at 21:14, 12 December 2012

OCA — Wed, 12 Dec 2012 21:14:45 GMT

←Older revision		Revision as of 21:14, 12 December 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:4hwj.jpg\|left\|200px]]

-	~~The entry~~ 4hwj ~~is ON HOLD~~	+	{{STRUCTURE_4hwj\| PDB=4hwj \| SCENE= }}

-	~~Authors: Bajic, G., Yatime, L., Andersen, G.R.~~	+	===Crystal Structure of the Human C3a desArg anaphylatoxin===

-	~~Description: Crystal~~ Structure ~~of the Human~~ C3a ~~desArg anaphylatoxin~~	+	{{ABSTRACT_PUBMED_23184394}}
		+
		+	==About this Structure==
		+	[[4hwj]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4HWJ OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Andersen, G R.]]
		+	[[Category: Bajic, G.]]
		+	[[Category: Yatime, L.]]
		+	[[Category: Anaphylatoxin]]
		+	[[Category: C3a]]
		+	[[Category: C3a desarg]]
		+	[[Category: C5a]]
		+	[[Category: C5a desarg]]
		+	[[Category: Complement system]]
		+	[[Category: Four-helix-bundle]]
		+	[[Category: Immune system]]
		+	[[Category: Inflammation]]
		+	[[Category: Innate immunity]]

OCA: Protected "4hwj" [edit=sysop:move=sysop]

OCA — Wed, 14 Nov 2012 06:21:10 GMT

Protected "4hwj" [edit=sysop:move=sysop]

←Older revision

Revision as of 06:21, 14 November 2012

OCA: New page: '''Unreleased structure''' The entry 4hwj is ON HOLD Authors: Bajic, G., Yatime, L., Andersen, G.R. Description: Crystal Structure of the Human C3a desArg anaphylatoxin

OCA — Wed, 14 Nov 2012 06:21:09 GMT

New page: '''Unreleased structure''' The entry 4hwj is ON HOLD Authors: Bajic, G., Yatime, L., Andersen, G.R. Description: Crystal Structure of the Human C3a desArg anaphylatoxin

New page

'''Unreleased structure'''

The entry 4hwj is ON HOLD

Authors: Bajic, G., Yatime, L., Andersen, G.R.

Description: Crystal Structure of the Human C3a desArg anaphylatoxin