2gsx - Revision history

OCA at 09:29, 14 February 2024

OCA — Wed, 14 Feb 2024 09:29:40 GMT

←Older revision		Revision as of 09:29, 14 February 2024
Line 3:		Line 3:
	<StructureSection load='2gsx' size='340' side='right'caption='[[2gsx]]' scene=''>		<StructureSection load='2gsx' size='340' side='right'caption='[[2gsx]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2GSX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2GSX FirstGlance]. <br>
-	</td></tr><tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~><div style='overflow: auto; max-height: 3em;'>[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</div></td></tr>~~	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray solution scattering</td></tr>
-	~~<tr~~ id~~='gene'><td class~~="~~sblockLbl~~">~~<b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([https://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'>[https://proteopedia.org/fgij/fg.htm?mol=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [https://pdbe.org/2gsx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [https://www.ebi.ac.uk/pdbsum/2gsx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2gsx ProSAT]</span></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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [https://pdbe.org/2gsx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [https://www.ebi.ac.uk/pdbsum/2gsx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2gsx ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[https://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[https://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>	+	[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[https://omim.org/entry/610927 610927]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[https://omim.org/entry/614699 614699]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>	+	[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2gsx ConSurf].		</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2gsx ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Complement receptor type 2 (CR2, CD21) is a cell surface protein that links the innate and adaptive immune response during the activation of B cells. The extracellular portion of CR2 comprises 15 or 16 short complement regulator (SCR) domains, for which the overall arrangement in solution is unknown. This was determined by constrained scattering and ultracentrifugation modelling. The radius of gyration of CR2 SCR 1-15 was determined to be 11.5 nm by both X-ray and neutron scattering, and that of its cross-section was 1.8 nm. The distance distribution function P(r) showed that the overall length of CR2 SCR 1-15 was 38 nm. Sedimentation equilibrium curve fits gave a mean molecular weight of 135,000 (+/- 13,000) Da, in agreement with a fully glycosylated structure. Velocity experiments using the g*(s) derivative method gave a sedimentation coefficient of 4.2 (+/- 0.1) S. In order to construct a model of CR2 SCR 1-15 for constrained fitting, homology models for the 15 SCR domains were combined with randomised linker peptides generated by molecular dynamics simulations. Using an automated procedure, the analysis of 15,000 possible CR2 SCR 1-15 models showed that only those models in which the 15 SCR domains were flexible but partially folded back accounted for the scattering and sedimentation data. The best-fit CR2 models provided a visual explanation for the versatile interaction of CR2 with four ligands C3d, CD23, gp350 and IFN-alpha. The flexible location of CR2 SCR 1-2 is likely to facilitate interactions of C3d-antigen complexes with the B cell receptor.
-
-	The 15 SCR flexible extracellular domains of human complement receptor type 2 can mediate multiple ligand and antigen interactions.,Gilbert HE, Asokan R, Holers VM, Perkins SJ J Mol Biol. 2006 Oct 6;362(5):1132-47. Epub 2006 Aug 9. PMID:16950392<ref>PMID:16950392</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 2gsx" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Asokan, R]]	+	[[Category: Asokan R]]
-	[[Category: Gilbert~~, H E~~]]	+	[[Category: Gilbert HE]]
-	[[Category: Holers~~, V M~~]]	+	[[Category: Holers VM]]
-	[[Category: Perkins~~, S J]]~~	+	[[Category: Perkins SJ]]
-	~~[[Category: Ccp domain]]~~	+
-	~~[[Category: Complement]]~~	+
-	~~[[Category: Immune system]]~~	+
-	~~[[Category: Scr domain]]~~	+
-	~~[[Category: Sushi domain~~]]	+

OCA at 19:16, 10 March 2021

OCA — Wed, 10 Mar 2021 19:16:42 GMT

←Older revision		Revision as of 19:16, 10 March 2021
Line 1:		Line 1:

	==Complement Receptor Type 2==		==Complement Receptor Type 2==
-	<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>	+	<StructureSection load='2gsx' size='340' side='right'caption='[[2gsx]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2GSX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2GSX FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([https://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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [~~http~~://pdbe.org/2gsx PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2gsx PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2gsx ProSAT]</span></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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [https://pdbe.org/2gsx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [https://www.ebi.ac.uk/pdbsum/2gsx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2gsx ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[~~http~~://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[~~http~~://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>	+	[[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[https://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[https://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>	+	[[https://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Asokan, R]]		[[Category: Asokan, R]]
	[[Category: Gilbert, H E]]		[[Category: Gilbert, H E]]

OCA at 07:52, 14 June 2018

OCA — Thu, 14 Jun 2018 07:52:12 GMT

←Older revision		Revision as of 07:52, 14 June 2018
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	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/gs/2gsx_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/gs/2gsx_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>

OCA at 08:00, 18 October 2017

OCA — Wed, 18 Oct 2017 08:00:22 GMT

←Older revision		Revision as of 08:00, 18 October 2017
Line 1:		Line 1:
		+
	==Complement Receptor Type 2==		==Complement Receptor Type 2==
	<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>		<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>
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	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://pdbe.org/2gsx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx 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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://pdbe.org/2gsx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2gsx ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 13:23, 9 February 2016

OCA — Tue, 09 Feb 2016 13:23:33 GMT

←Older revision		Revision as of 13:23, 9 February 2016
Line 19:		Line 19:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2gsx ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 22:39, 10 September 2015

OCA — Thu, 10 Sep 2015 22:39:13 GMT

←Older revision		Revision as of 22:39, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>		<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2GSX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2GSX FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([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">CR2, C3DR ([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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx 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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://pdbe.org/2gsx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 29:		Line 29:
	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 2gsx" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Asokan, R]]		[[Category: Asokan, R]]
	[[Category: Gilbert, H E]]		[[Category: Gilbert, H E]]

OCA at 08:19, 16 January 2015

OCA — Fri, 16 Jan 2015 08:19:59 GMT

←Older revision		Revision as of 08:19, 16 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2GSX FirstGlance]. <br>		<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2GSX FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([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">CR2, C3DR ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx 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=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[http://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[http://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>		[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[http://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[http://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
Line 34:		Line 34:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Asokan, R.]]	+	[[Category: Asokan, R]]
-	[[Category: Gilbert, H E.]]	+	[[Category: Gilbert, H E]]
-	[[Category: Holers, V M.]]	+	[[Category: Holers, V M]]
-	[[Category: Perkins, S J.]]	+	[[Category: Perkins, S J]]
	[[Category: Ccp domain]]		[[Category: Ccp domain]]
	[[Category: Complement]]		[[Category: Complement]]

OCA at 08:01, 30 September 2014

OCA — Tue, 30 Sep 2014 08:01:12 GMT

←Older revision		Revision as of 08:01, 30 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2gsx\| PDB~~=2gsx \| ~~SCENE~~= }}	+	==Complement Receptor Type 2==
-	===~~Complement~~ Receptor ~~Type 2~~===	+	<StructureSection load='2gsx' size='340' side='right' caption='[[2gsx]]' scene=''>
-	~~{{ABSTRACT_PUBMED_16950392}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2gsx]] 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=2GSX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2GSX FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ghq\|1ghq]], [[1w2r\|1w2r]], [[2aty\|2aty]]</td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CR2, C3DR ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2gsx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2gsx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2gsx RCSB], [http://www.ebi.ac.uk/pdbsum/2gsx PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[http://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[http://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/gs/2gsx_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Complement receptor type 2 (CR2, CD21) is a cell surface protein that links the innate and adaptive immune response during the activation of B cells. The extracellular portion of CR2 comprises 15 or 16 short complement regulator (SCR) domains, for which the overall arrangement in solution is unknown. This was determined by constrained scattering and ultracentrifugation modelling. The radius of gyration of CR2 SCR 1-15 was determined to be 11.5 nm by both X-ray and neutron scattering, and that of its cross-section was 1.8 nm. The distance distribution function P(r) showed that the overall length of CR2 SCR 1-15 was 38 nm. Sedimentation equilibrium curve fits gave a mean molecular weight of 135,000 (+/- 13,000) Da, in agreement with a fully glycosylated structure. Velocity experiments using the g*(s) derivative method gave a sedimentation coefficient of 4.2 (+/- 0.1) S. In order to construct a model of CR2 SCR 1-15 for constrained fitting, homology models for the 15 SCR domains were combined with randomised linker peptides generated by molecular dynamics simulations. Using an automated procedure, the analysis of 15,000 possible CR2 SCR 1-15 models showed that only those models in which the 15 SCR domains were flexible but partially folded back accounted for the scattering and sedimentation data. The best-fit CR2 models provided a visual explanation for the versatile interaction of CR2 with four ligands C3d, CD23, gp350 and IFN-alpha. The flexible location of CR2 SCR 1-2 is likely to facilitate interactions of C3d-antigen complexes with the B cell receptor.

-	~~==Disease==~~	+	The 15 SCR flexible extracellular domains of human complement receptor type 2 can mediate multiple ligand and antigen interactions.,Gilbert HE, Asokan R, Holers VM, Perkins SJ J Mol Biol. 2006 Oct 6;362(5):1132-47. Epub 2006 Aug 9. PMID:16950392<ref>PMID:16950392</ref>
-	~~[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus~~ type ~~9 (SLEB9) [MIM:[http://omim~~.~~org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory~~, ~~and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin~~, ~~joints~~, ~~kidneys~~, ~~and serosal membranes~~. ~~It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7~~ (~~CVID7~~) ~~[MIM~~:~~[http://omim~~.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:~~22035880~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd~~, ~~for~~ the ~~Epstein-Barr virus on human B-cells and T-cells and for HNRPU~~. ~~Participates in B lymphocytes activation~~.<~~ref~~>~~PMID:7753047~~</~~ref~~>	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[2gsx]] 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=2GSX OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:016950392</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Asokan, R.]]		[[Category: Asokan, R.]]

OCA at 09:39, 24 March 2013

OCA — Sun, 24 Mar 2013 09:39:36 GMT

←Older revision		Revision as of 09:39, 24 March 2013
Line 1:		Line 1:
-	[[Image:2gsx.png\|left\|200px]]
-
	{{STRUCTURE_2gsx\| PDB=2gsx \| SCENE= }}		{{STRUCTURE_2gsx\| PDB=2gsx \| SCENE= }}
-
	===Complement Receptor Type 2===		===Complement Receptor Type 2===
		+	{{ABSTRACT_PUBMED_16950392}}

-	~~{{ABSTRACT_PUBMED_16950392}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Genetic variations in CR2 are associated with susceptibility to systemic lupus erythematosus type 9 (SLEB9) [MIM:[http://omim.org/entry/610927 610927]]. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex genetic basis. SLE is an inflammatory, and often febrile multisystemic disorder of connective tissue characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:17360460</ref> Defects in CR2 are the cause of immunodeficiency, common variable, type 7 (CVID7) [MIM:[http://omim.org/entry/614699 614699]]. A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B cells is usually in the normal range, but can be low.<ref>PMID:22035880</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/CR2_HUMAN CR2_HUMAN]] Receptor for complement C3Dd, for the Epstein-Barr virus on human B-cells and T-cells and for HNRPU. Participates in B lymphocytes activation.<ref>PMID:7753047</ref>

	==About this Structure==		==About this Structure==
Line 11:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:016950392</ref><references group="xtra"/>	+	<ref group="xtra">PMID:016950392</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Asokan, R.]]		[[Category: Asokan, R.]]

OCA: Protected "2gsx" [edit=sysop:move=sysop]

OCA — Mon, 07 Jan 2013 18:05:17 GMT

Protected "2gsx" [edit=sysop:move=sysop]

←Older revision

Revision as of 18:05, 7 January 2013