3b3i - Revision history

OCA at 12:01, 30 August 2023

OCA — Wed, 30 Aug 2023 12:01:24 GMT

←Older revision		Revision as of 12:01, 30 August 2023
Line 3:		Line 3:
	<StructureSection load='3b3i' size='340' side='right'caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>		<StructureSection load='3b3i' size='340' side='right'caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3B3I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3B3I FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 1.86Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	~~<tr id~~='~~related'><td class~~=~~"sblockLbl"><b>[[Related_structure\|Related~~:~~]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;~~'>~~[[1ogt\|1ogt]], [[1of2\|1of2]]~~</~~div~~>~~</td></tr>~~	+
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), VIPR1 ([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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [https://pdbe.org/3b3i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [https://www.ebi.ac.uk/pdbsum/3b3i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3b3i 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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [https://pdbe.org/3b3i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [https://www.ebi.ac.uk/pdbsum/3b3i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3b3i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[https://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[https://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>	+	[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[https://omim.org/entry/241600 241600]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[https://www.uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38.<ref>PMID:8926282</ref> [[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.	+	[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 37:		Line 35:
	*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]		*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]
	*[[MHC 3D structures\|MHC 3D structures]]		*[[MHC 3D structures\|MHC 3D structures]]
		+	*[[MHC I 3D structures\|MHC I 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Beltrami, A]]	+	[[Category: Beltrami A]]
-	[[Category: Fiorillo~~, M T~~]]	+	[[Category: Fiorillo MT]]
-	[[Category: Kumar, P]]	+	[[Category: Kumar P]]
-	[[Category: Paladini, F]]	+	[[Category: Paladini F]]
-	[[Category: Rossmann, M]]	+	[[Category: Rossmann M]]
-	[[Category: Saenger, W]]	+	[[Category: Saenger W]]
-	[[Category: Sorrentino, R]]	+	[[Category: Sorrentino R]]
-	[[Category: Uchanska-Ziegler, B]]	+	[[Category: Uchanska-Ziegler B]]
-	[[Category: Ziegler, A]]	+	[[Category: Ziegler A]]
-	~~[[Category: Ankylosing spondylitis]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: G-protein coupled receptor]]~~	+
-	~~[[Category: Glycation]]~~	+
-	~~[[Category: Glycoprotein]]~~	+
-	~~[[Category: Hla-b2709]]~~	+
-	~~[[Category: Host-virus interaction]]~~	+
-	~~[[Category: Immune response]]~~	+
-	~~[[Category: Immune system]]~~	+
-	~~[[Category: Immunoglobulin domain]]~~	+
-	~~[[Category: Membrane]]~~	+
-	~~[[Category: Mhc i]]~~	+
-	~~[[Category: Phosphorylation]]~~	+
-	~~[[Category: Protein binding]]~~	+
-	~~[[Category: Pyrrolidone carboxylic acid]]~~	+
-	~~[[Category: Receptor]]~~	+
-	~~[[Category: Secreted]]~~	+
-	~~[[Category: Transducer]]~~	+
-	~~[[Category: Transmembrane~~]]	+

OCA at 11:22, 5 January 2022

OCA — Wed, 05 Jan 2022 11:22:36 GMT

←Older revision		Revision as of 11:22, 5 January 2022
Line 1:		Line 1:

	==Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes==		==Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes==
-	<StructureSection load='3b3i' size='340' side='right' caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>	+	<StructureSection load='3b3i' size='340' side='right'caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3B3I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3B3I FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1ogt\|1ogt]], [[1of2\|1of2]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), VIPR1 ([~~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">HLA-B, HLAB ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), VIPR1 ([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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [~~http~~://pdbe.org/3b3i PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3b3i PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3b3i 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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [https://pdbe.org/3b3i PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [https://www.ebi.ac.uk/pdbsum/3b3i PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3b3i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[~~http~~://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[~~http~~://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[~~http~~://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>	+	[[https://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[https://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[https://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[~~http~~://www.uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38.<ref>PMID:8926282</ref> [[~~http~~://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.	+	[[https://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[https://www.uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38.<ref>PMID:8926282</ref> [[https://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/b3/3b3i_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/b3/3b3i_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>
Line 33:		Line 33:
	</div>		</div>
	<div class="pdbe-citations 3b3i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3b3i" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Beta-2 microglobulin 3D structures\|Beta-2 microglobulin 3D structures]]
		+	*[[MHC 3D structures\|MHC 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 38:		Line 42:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Beltrami, A]]		[[Category: Beltrami, A]]
	[[Category: Fiorillo, M T]]		[[Category: Fiorillo, M T]]

OCA at 07:54, 25 October 2017

OCA — Wed, 25 Oct 2017 07:54:55 GMT

←Older revision		Revision as of 07:54, 25 October 2017
Line 33:		Line 33:
	</div>		</div>
	<div class="pdbe-citations 3b3i" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3b3i" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
-	*[[Major histocompatibility complex\|Major histocompatibility complex]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 09:32, 11 August 2016

OCA — Thu, 11 Aug 2016 09:32:49 GMT

←Older revision		Revision as of 09:32, 11 August 2016
Line 1:		Line 1:
		+
	==Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes==		==Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes==
	<StructureSection load='3b3i' size='340' side='right' caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>		<StructureSection load='3b3i' size='340' side='right' caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3B3I FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3B3I FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), B2M ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), VIPR1 ([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">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), B2M ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), VIPR1 ([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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [http://www.ebi.ac.uk/pdbsum/3b3i 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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [http://pdbe.org/3b3i PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [http://www.ebi.ac.uk/pdbsum/3b3i PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3b3i ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 21:		Line 22:
	<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=3b3i ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 31:		Line 32:
	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 3b3i" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 39:		Line 41:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Beltrami, A]]		[[Category: Beltrami, A]]
	[[Category: Fiorillo, M T]]		[[Category: Fiorillo, M T]]

OCA at 10:38, 20 January 2015

OCA — Tue, 20 Jan 2015 10:38:23 GMT

←Older revision		Revision as of 10:38, 20 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3B3I FirstGlance]. <br>		<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3B3I FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>	+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), VIPR1 ([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">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), VIPR1 ([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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [http://www.ebi.ac.uk/pdbsum/3b3i 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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [http://www.ebi.ac.uk/pdbsum/3b3i PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>		[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>
Line 40:		Line 40:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Beltrami, A.]]	+	[[Category: Beltrami, A]]
-	[[Category: Fiorillo, M T.]]	+	[[Category: Fiorillo, M T]]
-	[[Category: Kumar, P.]]	+	[[Category: Kumar, P]]
-	[[Category: Paladini, F.]]	+	[[Category: Paladini, F]]
-	[[Category: Rossmann, M.]]	+	[[Category: Rossmann, M]]
-	[[Category: Saenger, W.]]	+	[[Category: Saenger, W]]
-	[[Category: Sorrentino, R.]]	+	[[Category: Sorrentino, R]]
-	[[Category: Uchanska-Ziegler, B.]]	+	[[Category: Uchanska-Ziegler, B]]
-	[[Category: Ziegler, A.]]	+	[[Category: Ziegler, A]]
	[[Category: Ankylosing spondylitis]]		[[Category: Ankylosing spondylitis]]
	[[Category: Disease mutation]]		[[Category: Disease mutation]]

OCA at 05:02, 2 October 2014

OCA — Thu, 02 Oct 2014 05:02:13 GMT

←Older revision		Revision as of 05:02, 2 October 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3b3i~~\| ~~PDB~~=3b3i \| ~~SCENE~~= }}	+	==Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes==
-	===~~Citrullination~~-dependent ~~differential~~ presentation of a ~~self~~-peptide by ~~HLA~~-~~B27 subtypes~~===	+	<StructureSection load='3b3i' size='340' side='right' caption='[[3b3i]], [[Resolution\|resolution]] 1.86Å' scene=''>
-	~~{{ABSTRACT_PUBMED_18650441}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3b3i]] is a 3 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=3B3I OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3B3I FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=CIR:CITRULLINE'>CIR</scene></td></tr>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1ogt\|1ogt]], [[1of2\|1of2]]</td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">HLA-B, HLAB ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), B2M ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), VIPR1 ([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=3b3i FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3b3i OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3b3i RCSB], [http://www.ebi.ac.uk/pdbsum/3b3i PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref> <ref>PMID:1336137</ref> <ref>PMID:7554280</ref> <ref>PMID:4586824</ref> <ref>PMID:8084451</ref> <ref>PMID:12119416</ref> <ref>PMID:12796775</ref> <ref>PMID:16901902</ref> <ref>PMID:16491088</ref> <ref>PMID:17646174</ref> <ref>PMID:18835253</ref> <ref>PMID:18395224</ref> <ref>PMID:19284997</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38.<ref>PMID:8926282</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
		+	== 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/b3/3b3i_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 ==
		+	Inflammatory processes are accompanied by the posttranslational modification of certain arginine residues within proteins to yield citrulline, although it is largely unknown how this modification influences antigen presentation. We employed crystallographic and functional studies to investigate whether the exchange of arginine to citrulline affects the display of a peptide by two human major histocompatibility antigen class I subtypes, HLA-B()2705 and HLA-B()2709. Both differ only in residue 116 within the peptide binding groove despite their differential association with ankylosing spondylitis, an inflammatory rheumatic disorder. The crystal structures described here show that a modified self-peptide, pVIPR-U5 (RRKWURWHL; U = citrulline), is presented by the two HLA-B27 molecules in distinct conformations. These binding modes differ not only drastically from each other but also from the conformations exhibited by the non-citrullinated peptide in a given subtype. The differential reactivity of HLA-B27-restricted cytotoxic T cells with modified or unmodified pVIPR supports the structural findings and shows that the presentation of citrullinated peptides has the potential to influence immune responses.

-	~~==Disease==~~	+	Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes.,Beltrami A, Rossmann M, Fiorillo MT, Paladini F, Sorrentino R, Saenger W, Kumar P, Ziegler A, Uchanska-Ziegler B J Biol Chem. 2008 Oct 3;283(40):27189-99. Epub 2008 Jul 23. PMID:18650441<ref>PMID:18650441</ref>
-	~~[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA~~-~~B are a cause~~ of ~~susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is~~ a ~~chronic rheumatic disease with multifactorial inheritance~~. ~~It includes a spectrum of related disorders comprising ankylosing spondylitis~~, ~~a subset of psoriatic arthritis~~, ~~reactive arthritis (e.g. Reiter syndrome)~~, ~~arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient~~, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, ~~intervertebral~~, ~~and costovertebral joints. Note=In the Greek Cypriot population~~, ~~a restricted number of HLA~~-~~B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the~~ B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (~~HYCATHYP~~) ~~[MIM~~:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-~~2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states~~. ~~The capacity to assemble into amyloid fibrils is concentration dependent~~. ~~Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>~~PMID:3532124</ref><ref>PMID:1336137</ref><ref>PMID:7554280</ref><ref>PMID:4586824</ref><ref>PMID:8084451</ref><ref>PMID:12119416</ref><ref>PMID:12796775</ref><ref>PMID:16901902</ref><ref>PMID:16491088</ref><ref>PMID:17646174</ref><ref>PMID:18835253</ref><ref>PMID:18395224</ref><ref>PMID:~~19284997~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation~~ of ~~foreign antigens to~~ the ~~immune system~~. ~~[[http://www~~.~~uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity~~ of ~~this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38~~.<~~ref~~>~~PMID:8926282~~</~~ref~~> ~~[[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.~~	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[3b3i]] is a 3 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=3B3I OCA].	+

	==See Also==		==See Also==
	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]		*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
	*[[Major histocompatibility complex\|Major histocompatibility complex]]		*[[Major histocompatibility complex\|Major histocompatibility complex]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:018650441</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Beltrami, A.]]		[[Category: Beltrami, A.]]

OCA at 16:31, 24 March 2013

OCA — Sun, 24 Mar 2013 16:31:22 GMT

←Older revision		Revision as of 16:31, 24 March 2013
Line 1:		Line 1:
-	[[Image:3b3i.png\|left\|200px]]
-
	{{STRUCTURE_3b3i\| PDB=3b3i \| SCENE= }}		{{STRUCTURE_3b3i\| PDB=3b3i \| SCENE= }}
-
	===Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes===		===Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes===
		+	{{ABSTRACT_PUBMED_18650441}}

-	~~{{ABSTRACT_PUBMED_18650441}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Defects in HLA-B are a cause of susceptibility to spondyloarthropathy type 1 (SPDA1) [MIM:[http://omim.org/entry/106300 106300]]. It is a chronic rheumatic disease with multifactorial inheritance. It includes a spectrum of related disorders comprising ankylosing spondylitis, a subset of psoriatic arthritis, reactive arthritis (e.g. Reiter syndrome), arthritis associated with inflammatory bowel disease and undifferentiated spondyloarthropathy. These disorders may occur simultaneously or sequentially in the same patient, probably representing various phenotypic expressions of the same disease. Ankylosing spondylitis is the form of rheumatoid arthritis affecting the spine and is considered the prototype of seronegative spondyloarthropathies. It produces pain and stiffness as a result of inflammation of the sacroiliac, intervertebral, and costovertebral joints. Note=In the Greek Cypriot population, a restricted number of HLA-B27 subtypes are associated with ankylosing spondylitis and other B27-related diseases and an elevated frequency of the B2702 allele in ankylosing spondylitis patients is identified. The allele B2707 seems to have a protective role in this population because it was found only in the healthy controls.<ref>PMID:15603872</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Defects in B2M are the cause of hypercatabolic hypoproteinemia (HYCATHYP) [MIM:[http://omim.org/entry/241600 241600]]. Affected individuals show marked reduction in serum concentrations of immunoglobulin and albumin, probably due to rapid degradation.<ref>PMID:16549777</ref> Note=Beta-2-microglobulin may adopt the fibrillar configuration of amyloid in certain pathologic states. The capacity to assemble into amyloid fibrils is concentration dependent. Persistently high beta(2)-microglobulin serum levels lead to amyloidosis in patients on long-term hemodialysis.<ref>PMID:3532124</ref><ref>PMID:1336137</ref><ref>PMID:7554280</ref><ref>PMID:4586824</ref><ref>PMID:8084451</ref><ref>PMID:12119416</ref><ref>PMID:12796775</ref><ref>PMID:16901902</ref><ref>PMID:16491088</ref><ref>PMID:17646174</ref><ref>PMID:18835253</ref><ref>PMID:18395224</ref><ref>PMID:19284997</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/1B27_HUMAN 1B27_HUMAN]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/VIPR1_HUMAN VIPR1_HUMAN]] This is a receptor for VIP. The activity of this receptor is mediated by G proteins which activate adenylyl cyclase. The affinity is VIP = PACAP-27 > PACAP-38.<ref>PMID:8926282</ref> [[http://www.uniprot.org/uniprot/B2MG_HUMAN B2MG_HUMAN]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.

	==About this Structure==		==About this Structure==
Line 15:		Line 17:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:018650441</ref><references group="xtra"/>	+	<ref group="xtra">PMID:018650441</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Beltrami, A.]]		[[Category: Beltrami, A.]]

OCA at 18:51, 20 October 2012

OCA — Sat, 20 Oct 2012 18:51:25 GMT

←Older revision		Revision as of 18:51, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3b3i]] is a 3 chain structure ~~of [[Beta-2 microglobulin]] and [[Major histocompatibility complex]]~~ 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=3B3I OCA].	+	[[3b3i]] is a 3 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=3B3I OCA].

	==See Also==		==See Also==

OCA: Protected "3b3i" [edit=sysop:move=sysop]

OCA — Fri, 27 Jul 2012 05:28:52 GMT

Protected "3b3i" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:28, 27 July 2012

OCA at 05:28, 27 July 2012

OCA — Fri, 27 Jul 2012 05:28:50 GMT

←Older revision		Revision as of 05:28, 27 July 2012
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-	{{Seed}}
	[[Image:3b3i.png\|left\|200px]]		[[Image:3b3i.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3b3i", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
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	{{STRUCTURE_3b3i\| PDB=3b3i \| SCENE= }}		{{STRUCTURE_3b3i\| PDB=3b3i \| SCENE= }}

	===Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes===		===Citrullination-dependent differential presentation of a self-peptide by HLA-B27 subtypes===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_18650441}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 18650441 is the PubMed ID number.
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	{{ABSTRACT_PUBMED_18650441}}		{{ABSTRACT_PUBMED_18650441}}

-	==~~Disease~~==	+	==About this Structure==
-	~~Known disease associated with this~~ structure~~: Hypoproteinemia, hypercatabolic OMIM:~~[[http://~~www~~.~~ncbi~~.~~nlm~~.~~nih.gov~~/~~entrez~~/~~dispomim~~.~~cgi~~?id=~~109700 109700]~~]	+	[[3b3i]] is a 3 chain structure of [[Beta-2 microglobulin]] and [[Major histocompatibility complex]] 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=3B3I OCA].

-	==~~About this Structure~~==	+	==See Also==
-	~~3B3I is a 3 chains structure of sequences 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=3B3I OCA~~].	+	*[[Beta-2 microglobulin\|Beta-2 microglobulin]]
		+	*[[Major histocompatibility complex\|Major histocompatibility complex]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~18650441~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:018650441</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Beltrami, A.]]		[[Category: Beltrami, A.]]
Line 37:		Line 26:
	[[Category: Uchanska-Ziegler, B.]]		[[Category: Uchanska-Ziegler, B.]]
	[[Category: Ziegler, A.]]		[[Category: Ziegler, A.]]
-	[[Category: Alternative splicing]]
	[[Category: Ankylosing spondylitis]]		[[Category: Ankylosing spondylitis]]
	[[Category: Disease mutation]]		[[Category: Disease mutation]]
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	[[Category: Mhc i]]		[[Category: Mhc i]]
	[[Category: Phosphorylation]]		[[Category: Phosphorylation]]
-	[[Category: Polymorphism]]
	[[Category: Protein binding]]		[[Category: Protein binding]]
	[[Category: Pyrrolidone carboxylic acid]]		[[Category: Pyrrolidone carboxylic acid]]
Line 58:		Line 45:
	[[Category: Transducer]]		[[Category: Transducer]]
	[[Category: Transmembrane]]		[[Category: Transmembrane]]
-	[[Category: Ubl conjugation]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Feb 17 21:38:19 2009''