3up1 - Revision history

OCA at 10:00, 21 December 2022

2022-12-21T10:00:49Z

←Older revision		Revision as of 10:00, 21 December 2022
Line 3:		Line 3:
	<StructureSection load='3up1' size='340' side='right'caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>		<StructureSection load='3up1' size='340' side='right'caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=~~NGA~~:N-ACETYL-D-~~GALACTOSAMINE~~'>~~NGA~~</scene>, <scene name='pdbligand=~~SO4~~:~~SULFATE+ION~~'>~~SO4~~</scene>, <scene name='pdbligand=~~NAG~~:~~N-ACETYL-D-GLUCOSAMINE~~'>~~NAG~~</scene>~~</td></tr>~~	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IL7R ([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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [https://pdbe.org/3up1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [https://www.ebi.ac.uk/pdbsum/3up1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3up1 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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [https://pdbe.org/3up1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [https://www.ebi.ac.uk/pdbsum/3up1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3up1 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[https://omim.org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref> [:]<ref>PMID:15372022</ref> <ref>PMID:15489334</ref> <ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[https://omim.org/entry/612595 612595]]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>	+	[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[https://omim.org/entry/608971 608971]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref> [:]<ref>PMID:15372022</ref> <ref>PMID:15489334</ref> <ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[https://omim.org/entry/612595 612595]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).	+	[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 28:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Holland~~, P J~~]]	+	[[Category: Holland PJ]]
-	[[Category: McElroy~~, C A~~]]	+	[[Category: McElroy CA]]
-	[[Category: Walsh~~, S T.R]]~~	+	[[Category: Walsh STR]]
-	~~[[Category: Cytokine receptor]]~~	+
-	~~[[Category: Fibronectin type 3 fold]]~~	+
-	~~[[Category: Glycosylation]]~~	+
-	~~[[Category: Immune system]]~~	+
-	~~[[Category: Membrane and soluble~~]]	+

OCA at 07:54, 20 July 2022

2022-07-20T07:54:34Z

←Older revision		Revision as of 07:54, 20 July 2022
Line 1:		Line 1:

	==Crystal structure of the unliganded human interleukin-7 receptor extracellular domain==		==Crystal structure of the unliganded human interleukin-7 receptor extracellular domain==
-	<StructureSection load='3up1' size='340' side='right' caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>	+	<StructureSection load='3up1' size='340' side='right'caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IL7R ([~~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">IL7R ([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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [~~http~~://pdbe.org/3up1 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3up1 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3up1 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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [https://pdbe.org/3up1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [https://www.ebi.ac.uk/pdbsum/3up1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3up1 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[~~http~~://omim.org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref> [:]<ref>PMID:15372022</ref> <ref>PMID:15489334</ref> <ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[~~http~~://omim.org/entry/612595 612595]]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>	+	[[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[https://omim.org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref> [:]<ref>PMID:15372022</ref> <ref>PMID:15489334</ref> <ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[https://omim.org/entry/612595 612595]]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).	+	[[https://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 23:		Line 23:

	==See Also==		==See Also==
-	*[[Interleukin receptor\|Interleukin receptor]]	+	*[[Interleukin receptor 3D structures\|Interleukin receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 29:		Line 29:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Holland, P J]]		[[Category: Holland, P J]]
	[[Category: McElroy, C A]]		[[Category: McElroy, C A]]

OCA at 13:15, 5 August 2016

2016-08-05T13:15:36Z

←Older revision		Revision as of 13:15, 5 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of the unliganded human interleukin-7 receptor extracellular domain==		==Crystal structure of the unliganded human interleukin-7 receptor extracellular domain==
	<StructureSection load='3up1' size='340' side='right' caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>		<StructureSection load='3up1' size='340' side='right' caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IL7R ([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">IL7R ([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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [http://www.ebi.ac.uk/pdbsum/3up1 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=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [http://pdbe.org/3up1 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [http://www.ebi.ac.uk/pdbsum/3up1 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3up1 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 19:		Line 20:
	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 3up1" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 26:		Line 28:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Holland, P J]]		[[Category: Holland, P J]]
	[[Category: McElroy, C A]]		[[Category: McElroy, C A]]

OCA at 06:50, 21 December 2014

2014-12-21T06:50:17Z

←Older revision		Revision as of 06:50, 21 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3up1~~\| ~~PDB~~=3up1 \| ~~SCENE~~= }}	+	==Crystal structure of the unliganded human interleukin-7 receptor extracellular domain==
-	===~~Crystal~~ structure of the unliganded ~~human~~ interleukin-7 receptor extracellular domain~~===~~	+	<StructureSection load='3up1' size='340' side='right' caption='[[3up1]], [[Resolution\|resolution]] 2.15Å' scene=''>
-	~~{{ABSTRACT_PUBMED_22308406}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3up1]] is a 2 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=3UP1 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3UP1 FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=NGA:N-ACETYL-D-GALACTOSAMINE'>NGA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IL7R ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3up1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3up1 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3up1 RCSB], [http://www.ebi.ac.uk/pdbsum/3up1 PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[http://omim.org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref> [:]<ref>PMID:15372022</ref> <ref>PMID:15489334</ref> <ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[http://omim.org/entry/612595 612595]]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	We report here an unliganded receptor structure in the common gamma-chain (gamma(c)) family of receptors and cytokines. The crystal structure of the unliganded form of the interleukin-7 alpha receptor (IL-7Ralpha) extracellular domain (ECD) at 2.15 A resolution reveals a homodimer forming an "X" geometry looking down onto the cell surface with the C termini of the two chains separated by 110 A and the dimer interface comprising residues critical for IL-7 binding. Further biophysical studies indicate a weak association of the IL-7Ralpha ECDs but a stronger association between the gamma(c)/IL-7Ralpha ECDs, similar to previous studies of the full-length receptors on CD4(+) T cells. Based on these and previous results, we propose a molecular mechanism detailing the progression from the inactive IL-7Ralpha homodimer and IL-7Ralpha-gamma(c) heterodimer to the active IL-7-IL-7Ralpha-gamma(c) ternary complex whereby the two receptors undergo at least a 90 degrees rotation away from the cell surface, moving the C termini of IL-7Ralpha and gamma(c) from a distance of 110 A to less than 30 A at the cell surface. This molecular mechanism can be used to explain recently discovered IL-7- and gamma(c)-independent gain-of-function mutations in IL-7Ralpha from B- and T-cell acute lymphoblastic leukemia patients. The mechanism may also be applicable to other gamma(c) receptors that form inactive homodimers and heterodimers independent of their cytokines.

-	~~==Disease==~~	+	Structural reorganization of the interleukin-7 signaling complex.,McElroy CA, Holland PJ, Zhao P, Lim JM, Wells L, Eisenstein E, Walsh ST Proc Natl Acad Sci U S A. 2012 Feb 14;109(7):2503-8. Epub 2012 Jan 30. PMID:22308406<ref>PMID:22308406</ref>
-	~~[[http://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause~~ of ~~severe combined immunodeficiency autosomal recessive T~~-~~cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[http://omim~~.~~org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID)~~, ~~a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity~~, ~~leukopenia~~, ~~and low or absent antibody levels. Patients present in infancy recurrent~~, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref>[:]<ref>PMID:15372022</ref><ref>PMID:15489334</ref><ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[http://omim.org/entry/612595 612595]]. A multifactorial, ~~inflammatory~~, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A ~~polymorphism at position 244 strongly influences susceptibility to multiple sclerosis~~. ~~Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele~~ (~~Thr-244~~) ~~or 'T' allele (Ile~~-~~244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R~~. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:~~17660817~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www~~.~~uniprot~~.~~org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP)~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[3up1]] is a 2 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=3UP1 OCA].~~	+

	==See Also==		==See Also==
	*[[Interleukin receptor\|Interleukin receptor]]		*[[Interleukin receptor\|Interleukin receptor]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:022308406</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Holland, P J.]]	+	[[Category: Holland, P J]]
-	[[Category: McElroy, C A.]]	+	[[Category: McElroy, C A]]
-	[[Category: Walsh, S T.R.]]	+	[[Category: Walsh, S T.R]]
	[[Category: Cytokine receptor]]		[[Category: Cytokine receptor]]
	[[Category: Fibronectin type 3 fold]]		[[Category: Fibronectin type 3 fold]]

OCA at 22:58, 24 March 2013

2013-03-24T22:58:17Z

←Older revision		Revision as of 22:58, 24 March 2013
Line 1:		Line 1:
-	[[Image:3up1.png\|left\|200px]]
-
	{{STRUCTURE_3up1\| PDB=3up1 \| SCENE= }}		{{STRUCTURE_3up1\| PDB=3up1 \| SCENE= }}
-
	===Crystal structure of the unliganded human interleukin-7 receptor extracellular domain===		===Crystal structure of the unliganded human interleukin-7 receptor extracellular domain===
		+	{{ABSTRACT_PUBMED_22308406}}

-	~~{{ABSTRACT_PUBMED_22308406}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:[http://omim.org/entry/608971 608971]]. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:9843216</ref>[:]<ref>PMID:15372022</ref><ref>PMID:15489334</ref><ref>PMID:11023514</ref> Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3) [MIM:[http://omim.org/entry/612595 612595]]. A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheat, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.<ref>PMID:17660817</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/IL7RA_HUMAN IL7RA_HUMAN]] Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP).

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:022308406</ref><references group="xtra"/>	+	<ref group="xtra">PMID:022308406</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Holland, P J.]]		[[Category: Holland, P J.]]

OCA at 20:22, 20 October 2012

2012-10-20T20:22:04Z

←Older revision		Revision as of 20:22, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3up1]] is a 2 chain structure ~~of [[Interleukin receptor]]~~ 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=3UP1 OCA].	+	[[3up1]] is a 2 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=3UP1 OCA].

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

OCA at 05:02, 22 August 2012

2012-08-22T05:02:08Z

←Older revision		Revision as of 05:02, 22 August 2012
Line 5:		Line 5:
	===Crystal structure of the unliganded human interleukin-7 receptor extracellular domain===		===Crystal structure of the unliganded human interleukin-7 receptor extracellular domain===

		+	{{ABSTRACT_PUBMED_22308406}}

	==About this Structure==		==About this Structure==
Line 11:		Line 12:
	==See Also==		==See Also==
	*[[Interleukin receptor\|Interleukin receptor]]		*[[Interleukin receptor\|Interleukin receptor]]
		+
		+	==Reference==
		+	<ref group="xtra">PMID:022308406</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Holland, P J.]]		[[Category: Holland, P J.]]

OCA at 10:13, 27 July 2012

2012-07-27T10:13:33Z

←Older revision		Revision as of 10:13, 27 July 2012
Line 1:		Line 1:
-	[[Image:3up1.~~jpg~~\|left\|200px]]	+	[[Image:3up1.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3up1", 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),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_3up1\| PDB=3up1 \| SCENE= }}		{{STRUCTURE_3up1\| PDB=3up1 \| SCENE= }}

Line 13:		Line 7:

	==About this Structure==		==About this Structure==
-	[[3up1]] is a 2 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=3UP1 OCA].	+	[[3up1]] is a 2 chain structure of [[Interleukin receptor]] 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=3UP1 OCA].
		+
		+	==See Also==
		+	*[[Interleukin receptor\|Interleukin receptor]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Holland, P J.]]		[[Category: Holland, P J.]]

OCA at 06:41, 8 February 2012

2012-02-08T06:41:36Z

←Older revision		Revision as of 06:41, 8 February 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:3up1.jpg\|left\|200px]]

-	The ~~entry 3up1~~ is ~~ON HOLD until sometime in~~ the ~~future~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3up1", 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),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_3up1\| PDB=3up1 \| SCENE= }}

-	~~Authors: McElroy, C.A., Holland, P.J., Walsh, S.T.R.~~	+	===Crystal structure of the unliganded human interleukin-7 receptor extracellular domain===

-	~~Description: Crystal~~ structure ~~of the unliganded human interleukin~~-7 receptor ~~extracellular domain~~	+
		+	==About this Structure==
		+	[[3up1]] is a 2 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=3UP1 OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Holland, P J.]]
		+	[[Category: McElroy, C A.]]
		+	[[Category: Walsh, S T.R.]]
		+	[[Category: Cytokine receptor]]
		+	[[Category: Fibronectin type 3 fold]]
		+	[[Category: Glycosylation]]
		+	[[Category: Immune system]]
		+	[[Category: Membrane and soluble]]

OCA at 06:48, 1 February 2012

2012-02-01T06:48:56Z

←Older revision		Revision as of 06:48, 1 February 2012
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3up1 is ON HOLD	+	The entry 3up1 is ON HOLD until sometime in the future

	Authors: McElroy, C.A., Holland, P.J., Walsh, S.T.R.		Authors: McElroy, C.A., Holland, P.J., Walsh, S.T.R.

	Description: Crystal structure of the unliganded human interleukin-7 receptor extracellular domain		Description: Crystal structure of the unliganded human interleukin-7 receptor extracellular domain