3osw - Revision history

OCA at 10:36, 21 February 2024

OCA — Wed, 21 Feb 2024 10:36:12 GMT

←Older revision		Revision as of 10:36, 21 February 2024
Line 3:		Line 3:
	<StructureSection load='3osw' size='340' side='right'caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>		<StructureSection load='3osw' size='340' side='right'caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3OSW FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3OSW FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=PGO:S~~-1,2~~-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</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]] 2.55Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"><~~div style~~='~~overflow~~: ~~auto; max~~-~~height: 3em;~~'>~~[[3osi\|3osi]]~~</~~div~~><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>
-	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td>~~<td class="sblockDat">PPARG, NR1C3 ([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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [https://pdbe.org/3osw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [https://www.ebi.ac.uk/pdbsum/3osw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3osw 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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [https://pdbe.org/3osw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [https://www.ebi.ac.uk/pdbsum/3osw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3osw ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[https://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[https://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[https://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.	+	[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[https://omim.org/entry/601665 601665]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[https://omim.org/entry/604367 604367]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[https://omim.org/entry/137800 137800]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>	+	[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	BACKGROUND: The occurrence of halogenated analogues of the xeno-estrogen bisphenol-A (BPA) has been recently demonstrated both in environmental and human samples. These include brominated (e.g. tetrabromobisphenol-A; TBBPA) as well as chlorinated (e.g. tetrachlorobisphenol-A; TCBPA) bisphenols which are both flame retardants. Due to their structural homology with BPA, such chemicals are candidate endocrine disruptors. However, their possible target(s) within the nuclear hormone receptor (NHRs) superfamily has remained unknown. OBJECTIVES: We investigated whether BPA and halogenated analogues could be ligands of estrogen (ERs) and peroxysome proliferator-activated (PPARs) receptors and act as endocrine disrupting chemicals (EDCs). METHODS: The activity of compounds was studied using reporter cell lines expressing ERs and PPARs. The binding affinities to PPARgamma were measured by competitive binding assays with [3H]-rosiglitazone. We also investigated the impact of TBBPA and TCBPA on adipocyte differentiation using NIH3T3-L1 cells. Finally, the binding mode of halogenated BPAs to PPARgamma was determined by X-ray crystallography. RESULTS: Two major outcomes of this study are the demonstration that TBBPA and TCBPA are human, zebrafish and xenopus PPARgamma ligands and the discovery of the mechanism by which these chemicals bind to and activate PPARgamma. We also provide evidence that activation of ERalpha, ERbeta and PPARgamma depends on the halogenation degree of BPA analogues. The bulkier brominated BPA analogues, the greater their capability to activate PPARgamma and the weaker their estrogenic potential. CONCLUSIONS: Our results strongly suggest that poly-halogenated bisphenols could function as obesogens by acting as agonists able to disrupt physiological functions regulated by human or animal PPARgamma.	+
-		+
-	Peroxysome Proliferator-Activated Receptor gamma is a Target for Halogenated Analogues of Bisphenol-A.,Riu A, Grimaldi M, le Maire A, Bey G, Phillips K, Boulahtouf A, Perdu E, Zalko D, Bourguet W, Balaguer P Environ Health Perspect. 2011 May 11. PMID:21561829<ref>PMID:21561829</ref>	+
-		+
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class="pdbe-citations 3osw" style="background-color:#fffaf0;"></div~~>	+

	==See Also==		==See Also==
Line 29:		Line 19:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Bourguet, W]]	+	[[Category: Bourguet W]]
-	[[Category: Maire, A ~~le]]~~	+	[[Category: Le Maire A]]
-	~~[[Category: Ligand binding protein]]~~	+
-	~~[[Category: Transcription~~]]	+

OCA at 10:55, 18 May 2022

OCA — Wed, 18 May 2022 10:55:57 GMT

←Older revision		Revision as of 10:55, 18 May 2022
Line 3:		Line 3:
	<StructureSection load='3osw' size='340' side='right'caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>		<StructureSection load='3osw' size='340' side='right'caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3OSW FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3OSW FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3osi\|3osi]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3osi\|3osi]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PPARG, NR1C3 ([~~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">PPARG, NR1C3 ([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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [~~http~~://pdbe.org/3osw PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3osw PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3osw 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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [https://pdbe.org/3osw PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [https://www.ebi.ac.uk/pdbsum/3osw PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3osw ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[~~http~~://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[~~http~~://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[~~http~~://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.	+	[[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[https://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[https://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[https://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>	+	[[https://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 24:		Line 24:

	==See Also==		==See Also==
-	*[[Peroxisome ~~Proliferator~~-~~Activated Receptors~~\|Peroxisome ~~Proliferator~~-~~Activated Receptors~~]]	+	*[[Peroxisome proliferator-activated receptor 3D structures\|Peroxisome proliferator-activated receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:30, 17 July 2019

OCA — Wed, 17 Jul 2019 11:30:58 GMT

←Older revision		Revision as of 11:30, 17 July 2019
Line 1:		Line 1:

	==Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)==		==Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)==
-	<StructureSection load='3osw' size='340' side='right' caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>	+	<StructureSection load='3osw' size='340' side='right'caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3OSW FirstGlance]. <br>		<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3OSW FirstGlance]. <br>
Line 30:		Line 30:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Bourguet, W]]		[[Category: Bourguet, W]]
	[[Category: Maire, A le]]		[[Category: Maire, A le]]
	[[Category: Ligand binding protein]]		[[Category: Ligand binding protein]]
	[[Category: Transcription]]		[[Category: Transcription]]

OCA at 19:27, 4 August 2016

OCA — Thu, 04 Aug 2016 19:27:46 GMT

←Older revision		Revision as of 19:27, 4 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)==		==Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)==
	<StructureSection load='3osw' size='340' side='right' caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>		<StructureSection load='3osw' size='340' side='right' caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3OSW FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3OSW FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3osi\|3osi]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3osi\|3osi]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PPARG, NR1C3 ([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">PPARG, NR1C3 ([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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [http://www.ebi.ac.uk/pdbsum/3osw 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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [http://pdbe.org/3osw PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [http://www.ebi.ac.uk/pdbsum/3osw PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3osw ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 21:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 3osw" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 27:		Line 29:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Bourguet, W]]		[[Category: Bourguet, W]]
	[[Category: Maire, A le]]		[[Category: Maire, A le]]
	[[Category: Ligand binding protein]]		[[Category: Ligand binding protein]]
	[[Category: Transcription]]		[[Category: Transcription]]

OCA at 06:55, 19 December 2014

OCA — Fri, 19 Dec 2014 06:55:00 GMT

←Older revision		Revision as of 06:55, 19 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3osw\| PDB=3osw \| SCENE= }}~~	+	==Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)==
-	===Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)===	+	<StructureSection load='3osw' size='340' side='right' caption='[[3osw]], [[Resolution\|resolution]] 2.55Å' scene=''>
-	~~{{ABSTRACT_PUBMED_21561829}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3osw]] 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=3OSW OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3OSW FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PGO:S-1,2-PROPANEDIOL'>PGO</scene>, <scene name='pdbligand=XDI:4,4-PROPANE-2,2-DIYLBIS(2,6-DIBROMOPHENOL)'>XDI</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3osi\|3osi]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PPARG, NR1C3 ([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=3osw FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3osw OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3osw RCSB], [http://www.ebi.ac.uk/pdbsum/3osw PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[http://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[http://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[http://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.		[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[http://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[http://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[http://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	BACKGROUND: The occurrence of halogenated analogues of the xeno-estrogen bisphenol-A (BPA) has been recently demonstrated both in environmental and human samples. These include brominated (e.g. tetrabromobisphenol-A; TBBPA) as well as chlorinated (e.g. tetrachlorobisphenol-A; TCBPA) bisphenols which are both flame retardants. Due to their structural homology with BPA, such chemicals are candidate endocrine disruptors. However, their possible target(s) within the nuclear hormone receptor (NHRs) superfamily has remained unknown. OBJECTIVES: We investigated whether BPA and halogenated analogues could be ligands of estrogen (ERs) and peroxysome proliferator-activated (PPARs) receptors and act as endocrine disrupting chemicals (EDCs). METHODS: The activity of compounds was studied using reporter cell lines expressing ERs and PPARs. The binding affinities to PPARgamma were measured by competitive binding assays with [3H]-rosiglitazone. We also investigated the impact of TBBPA and TCBPA on adipocyte differentiation using NIH3T3-L1 cells. Finally, the binding mode of halogenated BPAs to PPARgamma was determined by X-ray crystallography. RESULTS: Two major outcomes of this study are the demonstration that TBBPA and TCBPA are human, zebrafish and xenopus PPARgamma ligands and the discovery of the mechanism by which these chemicals bind to and activate PPARgamma. We also provide evidence that activation of ERalpha, ERbeta and PPARgamma depends on the halogenation degree of BPA analogues. The bulkier brominated BPA analogues, the greater their capability to activate PPARgamma and the weaker their estrogenic potential. CONCLUSIONS: Our results strongly suggest that poly-halogenated bisphenols could function as obesogens by acting as agonists able to disrupt physiological functions regulated by human or animal PPARgamma.

-	~~==Function==~~	+	Peroxysome Proliferator-Activated Receptor gamma is a Target for Halogenated Analogues of Bisphenol-A.,Riu A, Grimaldi M, le Maire A, Bey G, Phillips K, Boulahtouf A, Perdu E, Zalko D, Bourguet W, Balaguer P Environ Health Perspect. 2011 May 11. PMID:21561829<ref>PMID:21561829</ref>
-	~~[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]]~~ Receptor ~~that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by~~ a ~~ligand, the receptor binds to a promoter element in the gene~~ for ~~acyl~~-~~CoA oxidase and activates its transcription~~. ~~It therefore controls the peroxisomal beta-oxidation pathway of fatty acids~~. ~~Key regulator of adipocyte differentiation and glucose homeostasis~~. ~~Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>~~PMID:~~9065481</ref> <ref>PMID:16150867</ref>~~ <ref>PMID:~~20829347~~</ref>	+

-	~~==About this Structure==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[3osw]] 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=3OSW OCA].~~	+	</div>

-	==~~Reference~~==	+	==See Also==
-	~~<ref group~~=~~"xtra">PMID:021561829</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Bourguet, W.]]	+	[[Category: Bourguet, W]]
-	[[Category: Maire, A le.]]	+	[[Category: Maire, A le]]
	[[Category: Ligand binding protein]]		[[Category: Ligand binding protein]]
	[[Category: Transcription]]		[[Category: Transcription]]

OCA at 07:36, 20 June 2013

OCA — Thu, 20 Jun 2013 07:36:03 GMT

←Older revision		Revision as of 07:36, 20 June 2013
Line 4:		Line 4:

	==Disease==		==Disease==
-	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[http://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[http://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref><ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[http://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.	+	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[http://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[http://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref> <ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[http://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.

	==Function==		==Function==
-	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref><ref>PMID:16150867</ref><ref>PMID:20829347</ref>	+	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref> <ref>PMID:16150867</ref> <ref>PMID:20829347</ref>

	==About this Structure==		==About this Structure==
	[[3osw]] 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=3OSW OCA].		[[3osw]] 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=3OSW OCA].
-
-	==See Also==
-	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]

	==Reference==		==Reference==

OCA at 01:23, 25 March 2013

OCA — Mon, 25 Mar 2013 01:23:34 GMT

←Older revision		Revision as of 01:23, 25 March 2013
Line 1:		Line 1:
-	[[Image:3osw.png\|left\|200px]]
-
	{{STRUCTURE_3osw\| PDB=3osw \| SCENE= }}		{{STRUCTURE_3osw\| PDB=3osw \| SCENE= }}
-
	===Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)===		===Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)===
		+	{{ABSTRACT_PUBMED_21561829}}

-	~~{{ABSTRACT_PUBMED_21561829}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer. Defects in PPARG may be associated with susceptibility to obesity (OBESITY) [MIM:[http://omim.org/entry/601665 601665]]. It is a condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat.<ref>PMID:9753710</ref> Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:[http://omim.org/entry/604367 604367]]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia.<ref>PMID:12453919</ref><ref>PMID:11788685</ref> Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM:[http://omim.org/entry/137800 137800]]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas. Note=Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/PPARG_HUMAN PPARG_HUMAN]] Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses.<ref>PMID:9065481</ref><ref>PMID:16150867</ref><ref>PMID:20829347</ref>

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:021561829</ref><references group="xtra"/>	+	<ref group="xtra">PMID:021561829</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Bourguet, W.]]		[[Category: Bourguet, W.]]

OCA at 16:37, 20 October 2012

OCA — Sat, 20 Oct 2012 16:37:51 GMT

←Older revision		Revision as of 16:37, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3osw]] is a 2 chain structure ~~of [[Peroxisome Proliferator-Activated Receptors]]~~ 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=3OSW OCA].	+	[[3osw]] 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=3OSW OCA].

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

OCA at 22:18, 26 July 2012

OCA — Thu, 26 Jul 2012 22:18:45 GMT

←Older revision		Revision as of 22:18, 26 July 2012
Line 1:		Line 1:
-	[[Image:3osw.~~jpg~~\|left\|200px]]	+	[[Image:3osw.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3osw", 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.
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	{{STRUCTURE_3osw\| PDB=3osw \| SCENE= }}		{{STRUCTURE_3osw\| PDB=3osw \| SCENE= }}

	===Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)===		===Crystal structure of PPARgamma ligand binding domain in complex with tetrabromo-bisphenol A (TBBPA)===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_21561829}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 21561829 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_21561829}}		{{ABSTRACT_PUBMED_21561829}}

	==About this Structure==		==About this Structure==
-	[[3osw]] 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=3OSW OCA].	+	[[3osw]] is a 2 chain structure of [[Peroxisome Proliferator-Activated Receptors]] 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=3OSW OCA].
		+
		+	==See Also==
		+	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]

	==Reference==		==Reference==
Line 26:		Line 18:
	[[Category: Bourguet, W.]]		[[Category: Bourguet, W.]]
	[[Category: Maire, A le.]]		[[Category: Maire, A le.]]
		+	[[Category: Ligand binding protein]]
		+	[[Category: Transcription]]

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

OCA — Wed, 25 May 2011 05:37:10 GMT

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

←Older revision

Revision as of 05:37, 25 May 2011