2f4b - Revision history

OCA at 13:50, 13 March 2024

2024-03-13T13:50:23Z

← Older revision		Revision as of 13:50, 13 March 2024
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	<StructureSection load='2f4b' size='340' side='right'caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>		<StructureSection load='2f4b' size='340' side='right'caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</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]] 2.07Å</td></tr>
			<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [https://pdbe.org/2f4b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [https://www.ebi.ac.uk/pdbsum/2f4b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2f4b 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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [https://pdbe.org/2f4b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [https://www.ebi.ac.uk/pdbsum/2f4b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2f4b 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>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2f4b 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=2f4b ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	~~<div style="background-color:#fffaf0;">~~
	~~== Publication Abstract from PubMed ==~~
	A series of novel indole-based PPAR agonists is described leading to discovery of 10k, a highly potent PPAR pan-agonist. The structural biology and molecular docking studies revealed that the distances between the acidic group and the linker, when a ligand was complexed with PPARgamma protein, were important for the potent activity. The hydrophobic tail part of 10k makes intensive hydrophobic interaction with the PPARgamma protein resulting in potent activity.

	Indol-1-yl acetic acids as peroxisome proliferator-activated receptor agonists: design, synthesis, structural biology, and molecular docking studies.,Mahindroo N, Wang CC, Liao CC, Huang CF, Lu IL, Lien TW, Peng YH, Huang WJ, Lin YT, Hsu MC, Lin CH, Tsai CH, Hsu JT, Chen X, Lyu PC, Chao YS, Wu SY, Hsieh HP J Med Chem. 2006 Feb 9;49(3):1212-6. PMID:16451087<ref>PMID:16451087</ref>

	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~
	~~</div>~~
	~~<div class="pdbe-citations 2f4b" style="background-color:#fffaf0;"></div>~~

	==See Also==		==See Also==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Hsieh~~, H P~~]]		[[Category: Hsieh HP]]
	[[Category: Lu~~, I L~~]]		[[Category: Lu IL]]
	[[Category: Mahindroo, N]]		[[Category: Mahindroo N]]
	[[Category: Peng~~, Y H~~]]		[[Category: Peng YH]]
	[[Category: Wu~~, S Y]]~~		[[Category: Wu SY]]
	~~[[Category: Ppar]]~~
	~~[[Category: Transcription activator~~]]

OCA at 16:00, 22 December 2021

2021-12-22T16:00:48Z

← Older revision		Revision as of 16:00, 22 December 2021
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	<StructureSection load='2f4b' size='340' side='right'caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>		<StructureSection load='2f4b' size='340' side='right'caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [~~http~~://pdbe.org/2f4b PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2f4b PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2f4b 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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [https://pdbe.org/2f4b PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [https://www.ebi.ac.uk/pdbsum/2f4b PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2f4b 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>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	==See Also==		==See Also==
	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]		*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
	*[[~~Phenylethanolamine N~~-~~methyltransferase~~ 3D structures\|~~Phenylethanolamine N~~-~~methyltransferase~~ 3D structures]]		*[[Peroxisome proliferator-activated receptor 3D structures\|Peroxisome proliferator-activated receptor 3D structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 10:45, 18 March 2020

2020-03-18T10:45:29Z

← Older revision		Revision as of 10:45, 18 March 2020
Line 1:		Line 1:

	==Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist==		==Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist==
	<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>		<StructureSection load='2f4b' size='340' side='right'caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
Line 33:		Line 33:
	==See Also==		==See Also==
	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]		*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
			*[[Phenylethanolamine N-methyltransferase 3D structures\|Phenylethanolamine N-methyltransferase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
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	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Hsieh, H P]]		[[Category: Hsieh, H P]]
	[[Category: Lu, I L]]		[[Category: Lu, I L]]

OCA at 08:47, 14 June 2018

2018-06-14T08:47:10Z

← Older revision		Revision as of 08:47, 14 June 2018
Line 1:		Line 1:

	==Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist==		==Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist==
	<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>		<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
Line 4:		Line 5:
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://pdbe.org/2f4b PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b 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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://pdbe.org/2f4b PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2f4b ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 14:		Line 15:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/f4/2f4b_consurf.spt"</scriptWhenChecked>		<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/f4/2f4b_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 13:03, 8 February 2016

2016-02-08T13:03:28Z

← Older revision		Revision as of 13:03, 8 February 2016
Line 18:		Line 18:
	<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=2f4b ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 11:50, 10 September 2015

2015-09-10T11:50:59Z

← Older revision		Revision as of 11:50, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>		<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b 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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://pdbe.org/2f4b PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 28:		Line 28:
	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 2f4b" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 35:		Line 36:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Homo sapiens~~]]		[[Category: Human]]
	[[Category: Hsieh, H P]]		[[Category: Hsieh, H P]]
	[[Category: Lu, I L]]		[[Category: Lu, I L]]

OCA at 08:14, 16 January 2015

2015-01-16T08:14:53Z

← Older revision		Revision as of 08:14, 16 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>		<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene><br>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene></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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b 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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b PDBsum]</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.		[[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.
Line 36:		Line 36:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hsieh, H P.]]		[[Category: Hsieh, H P]]
	[[Category: Lu, I L.]]		[[Category: Lu, I L]]
	[[Category: Mahindroo, N.]]		[[Category: Mahindroo, N]]
	[[Category: Peng, Y H.]]		[[Category: Peng, Y H]]
	[[Category: Wu, S Y.]]		[[Category: Wu, S Y]]
	[[Category: Ppar]]		[[Category: Ppar]]
	[[Category: Transcription activator]]		[[Category: Transcription activator]]

OCA at 01:47, 30 September 2014

2014-09-30T01:47:13Z

← Older revision		Revision as of 01:47, 30 September 2014
Line 1:		Line 1:
	~~{{STRUCTURE_2f4b\| PDB=2f4b \| SCENE= }}~~		==Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist==
	===Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist===		<StructureSection load='2f4b' size='340' side='right' caption='[[2f4b]], [[Resolution\|resolution]] 2.07Å' scene=''>
	{~~{ABSTRACT_PUBMED_16451087}~~}		== Structural highlights ==
			<table><tr><td colspan='2'>[[2f4b]] 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=2F4B OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2F4B FirstGlance]. <br>
			</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EHA:(5-{3-[(6-BENZOYL-1-PROPYL-2-NAPHTHYL)OXY]PROPOXY}-1H-INDOL-1-YL)ACETIC+ACID'>EHA</scene><br>
			<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=2f4b FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2f4b OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2f4b RCSB], [http://www.ebi.ac.uk/pdbsum/2f4b 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.
			== 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>
			== 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/f4/2f4b_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 ==
			A series of novel indole-based PPAR agonists is described leading to discovery of 10k, a highly potent PPAR pan-agonist. The structural biology and molecular docking studies revealed that the distances between the acidic group and the linker, when a ligand was complexed with PPARgamma protein, were important for the potent activity. The hydrophobic tail part of 10k makes intensive hydrophobic interaction with the PPARgamma protein resulting in potent activity.

	~~==Disease==~~		Indol-1-yl acetic acids as peroxisome proliferator-activated receptor agonists: design, synthesis, structural biology, and molecular docking studies.,Mahindroo N, Wang CC, Liao CC, Huang CF, Lu IL, Lien TW, Peng YH, Huang WJ, Lin YT, Hsu MC, Lin CH, Tsai CH, Hsu JT, Chen X, Lyu PC, Chao YS, Wu SY, Hsieh HP J Med Chem. 2006 Feb 9;49(3):1212-6. PMID:16451087<ref>PMID:16451087</ref>
	~~[[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==~~		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	~~[[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>

	~~==About this Structure==~~
	[[2f4b]] 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=2F4B OCA].

	==See Also==		==See Also==
	*[[PPAR-gamma\|PPAR-gamma]]
	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]		*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
			== References ==
	==~~Reference~~==		<references/>
	~~<ref group="xtra">PMID:016451087</ref>~~<references ~~group="xtra"~~/><~~references~~/>		__TOC__
			</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hsieh, H P.]]		[[Category: Hsieh, H P.]]

OCA at 16:10, 24 March 2013

2013-03-24T16:10:39Z

← Older revision		Revision as of 16:10, 24 March 2013
Line 2:		Line 2:
	===Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist===		===Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist===
	{{ABSTRACT_PUBMED_16451087}}		{{ABSTRACT_PUBMED_16451087}}

			==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 11:		Line 17:

	==Reference==		==Reference==
	<ref group="xtra">PMID:016451087</ref><references group="xtra"/>		<ref group="xtra">PMID:016451087</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hsieh, H P.]]		[[Category: Hsieh, H P.]]

OCA at 10:23, 11 March 2013

2013-03-11T10:23:19Z

← Older revision		Revision as of 10:23, 11 March 2013
Line 1:		Line 1:
	~~[[Image:2f4b.png\|left\|200px]]~~

	{{STRUCTURE_2f4b\| PDB=2f4b \| SCENE= }}		{{STRUCTURE_2f4b\| PDB=2f4b \| SCENE= }}

	===Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist===		===Crystal structure of the ligand binding domain of human PPAR-gamma in complex with an agonist===

	{{ABSTRACT_PUBMED_16451087}}		{{ABSTRACT_PUBMED_16451087}}