4a4w - Revision history

OCA at 11:19, 20 December 2023

OCA — Wed, 20 Dec 2023 11:19:41 GMT

←Older revision		Revision as of 11:19, 20 December 2023
Line 3:		Line 3:
	<StructureSection load='4a4w' size='340' side='right'caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='4a4w' size='340' side='right'caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4A4W FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4A4W FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=YFB:AMORFRUTIN+B'>YFB</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]] 2Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"><~~div style~~='~~overflow~~: ~~auto; max-height: 3em;~~'>[[2fvj\|2fvj]], [[2xkw\|2xkw]], [[2vv2\|2vv2]], [[1fm9\|1fm9]], [[2vv0\|2vv0]], [[2vv1\|2vv1]], [[2prg\|2prg]], [[1knu\|1knu]], [[1rdt\|1rdt]], [[2vv4\|2vv4]], [[3prg\|3prg]], [[1i7i\|1i7i]], [[1k74\|1k74]], [[1fm6\|1fm6]], [[1prg\|1prg]], [[1zgy\|1zgy]], [[2f4b\|2f4b]], [[2vst\|2vst]], [[2g0h\|2g0h]], [[2vsr\|2vsr]], [[1wm0\|1wm0]], [[4prg\|4prg]], [[2g0g\|2g0g]], [[1nyx\|1nyx]], [[2vv3\|2vv3]], [[2yfe\|2yfe]], [[4a4v\|4a4v]]</~~div~~></td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=YFB:AMORFRUTIN+B'>YFB</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=4a4w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4a4w OCA], [https://pdbe.org/4a4w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4a4w RCSB], [https://www.ebi.ac.uk/pdbsum/4a4w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4a4w 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=4a4w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4a4w OCA], [https://pdbe.org/4a4w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4a4w RCSB], [https://www.ebi.ac.uk/pdbsum/4a4w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4a4w 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;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 28:		Line 28:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Buessow, K]]	+	[[Category: Buessow K]]
-	~~[[Category: Groot, J C.de~~]]	+	[[Category: Kawamoto K]]
-	[[Category: Kawamoto, K]]	+	[[Category: Krausze J]]
-	[[Category: Krausze, J]]	+	[[Category: Sauer S]]
-	[[Category: Sauer, S]]	+	[[Category: Schroeder FC]]
-	[[Category: Schroeder~~, F C~~]]	+	[[Category: Weidner C]]
-	[[Category: Weidner, C]]	+	[[Category: De Groot JC]]
-	[[Category: ~~Agonist]]~~	+
-	~~[[Category: Diabetes]]~~	+
-	~~[[Category: Insulin resistance]]~~	+
-	~~[[Category: Receptor~~]]	+

OCA at 07:45, 18 August 2022

OCA — Thu, 18 Aug 2022 07:45:28 GMT

←Older revision		Revision as of 07:45, 18 August 2022
Line 3:		Line 3:
	<StructureSection load='4a4w' size='340' side='right'caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>		<StructureSection load='4a4w' size='340' side='right'caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=4A4W FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4A4W FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=YFB:AMORFRUTIN+B'>YFB</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=YFB:AMORFRUTIN+B'>YFB</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fvj\|2fvj]], [[2xkw\|2xkw]], [[2vv2\|2vv2]], [[1fm9\|1fm9]], [[2vv0\|2vv0]], [[2vv1\|2vv1]], [[2prg\|2prg]], [[1knu\|1knu]], [[1rdt\|1rdt]], [[2vv4\|2vv4]], [[3prg\|3prg]], [[1i7i\|1i7i]], [[1k74\|1k74]], [[1fm6\|1fm6]], [[1prg\|1prg]], [[1zgy\|1zgy]], [[2f4b\|2f4b]], [[2vst\|2vst]], [[2g0h\|2g0h]], [[2vsr\|2vsr]], [[1wm0\|1wm0]], [[4prg\|4prg]], [[2g0g\|2g0g]], [[1nyx\|1nyx]], [[2vv3\|2vv3]], [[2yfe\|2yfe]], [[4a4v\|4a4v]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2fvj\|2fvj]], [[2xkw\|2xkw]], [[2vv2\|2vv2]], [[1fm9\|1fm9]], [[2vv0\|2vv0]], [[2vv1\|2vv1]], [[2prg\|2prg]], [[1knu\|1knu]], [[1rdt\|1rdt]], [[2vv4\|2vv4]], [[3prg\|3prg]], [[1i7i\|1i7i]], [[1k74\|1k74]], [[1fm6\|1fm6]], [[1prg\|1prg]], [[1zgy\|1zgy]], [[2f4b\|2f4b]], [[2vst\|2vst]], [[2g0h\|2g0h]], [[2vsr\|2vsr]], [[1wm0\|1wm0]], [[4prg\|4prg]], [[2g0g\|2g0g]], [[1nyx\|1nyx]], [[2vv3\|2vv3]], [[2yfe\|2yfe]], [[4a4v\|4a4v]]</div></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=4a4w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4a4w OCA], [~~http~~://pdbe.org/4a4w PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=4a4w RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/4a4w PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=4a4w 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=4a4w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4a4w OCA], [https://pdbe.org/4a4w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4a4w RCSB], [https://www.ebi.ac.uk/pdbsum/4a4w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4a4w 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 23:		Line 23:

	==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/>
Line 29:		Line 29:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Buessow, K]]		[[Category: Buessow, K]]
	[[Category: Groot, J C.de]]		[[Category: Groot, J C.de]]

OCA at 09:15, 6 March 2019

OCA — Wed, 06 Mar 2019 09:15:45 GMT

←Older revision		Revision as of 09:15, 6 March 2019
Line 1:		Line 1:

	==Ligand binding domain of human PPAR gamma in complex with amorfrutin B==		==Ligand binding domain of human PPAR gamma in complex with amorfrutin B==
-	<StructureSection load='4a4w' size='340' side='right' caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>	+	<StructureSection load='4a4w' size='340' side='right'caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4A4W FirstGlance]. <br>		<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4A4W FirstGlance]. <br>

OCA at 11:29, 4 August 2016

OCA — Thu, 04 Aug 2016 11:29:05 GMT

←Older revision		Revision as of 11:29, 4 August 2016
Line 1:		Line 1:
-	{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}
-	===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===
-	{{ABSTRACT_PUBMED_23286787}}

-	==Disease==	+	==Ligand binding domain of human PPAR gamma in complex with amorfrutin B==
		+	<StructureSection load='4a4w' size='340' side='right' caption='[[4a4w]], [[Resolution\|resolution]] 2.00Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[4a4w]] 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=4A4W OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4A4W FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=YFB:AMORFRUTIN+B'>YFB</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2fvj\|2fvj]], [[2xkw\|2xkw]], [[2vv2\|2vv2]], [[1fm9\|1fm9]], [[2vv0\|2vv0]], [[2vv1\|2vv1]], [[2prg\|2prg]], [[1knu\|1knu]], [[1rdt\|1rdt]], [[2vv4\|2vv4]], [[3prg\|3prg]], [[1i7i\|1i7i]], [[1k74\|1k74]], [[1fm6\|1fm6]], [[1prg\|1prg]], [[1zgy\|1zgy]], [[2f4b\|2f4b]], [[2vst\|2vst]], [[2g0h\|2g0h]], [[2vsr\|2vsr]], [[1wm0\|1wm0]], [[4prg\|4prg]], [[2g0g\|2g0g]], [[1nyx\|1nyx]], [[2vv3\|2vv3]], [[2yfe\|2yfe]], [[4a4v\|4a4v]]</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=4a4w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4a4w OCA], [http://pdbe.org/4a4w PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4a4w RCSB], [http://www.ebi.ac.uk/pdbsum/4a4w PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4a4w ProSAT]</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 ==
-	==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>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Amorfrutins are a family of natural products with high affinity to the peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor regulating lipid and glucose metabolism. The PPARgamma agonist rosiglitazone increases insulin sensitivity and is effective against type II diabetes but has severe adverse effects including weight gain. Amorfrutins improve insulin sensitivity and dyslipidemia but do not enhance undesired fat storage. They bear potential as therapeutics or prophylactic dietary supplements. We identified amorfrutin B as a novel partial agonist of PPARgamma with a considerably higher affinity than that of previously reported amorfrutins, similar to that of rosiglitazone. Crystal structures reveal the geranyl side chain of amorfrutin B as the cause of its particularly high affinity. Typical for partial agonists, amorfrutins 1, 2, and B bind helix H3 and the beta-sheet of PPARgamma but not helix H12.
		+
		+	Structural characterization of amorfrutins bound to the peroxisome proliferator-activated receptor gamma.,de Groot JC, Weidner C, Krausze J, Kawamoto K, Schroeder FC, Sauer S, Bussow K J Med Chem. 2013 Feb 28;56(4):1535-43. doi: 10.1021/jm3013272. Epub 2013 Feb 6. PMID:23286787<ref>PMID:23286787</ref>

-	~~==About this Structure==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[4a4w]] 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=4A4W OCA].~~	+	</div>
		+	<div class="pdbe-citations 4a4w" style="background-color:#fffaf0;"></div>

-	==~~Reference~~==	+	==See Also==
-	~~<ref group~~=~~"xtra">PMID:023286787</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Human]]		[[Category: Human]]
-	[[Category: Buessow, K.]]	+	[[Category: Buessow, K]]
-	[[Category: Groot, J C.de.]]	+	[[Category: Groot, J C.de]]
-	[[Category: Kawamoto, K.]]	+	[[Category: Kawamoto, K]]
-	[[Category: Krausze, J.]]	+	[[Category: Krausze, J]]
-	[[Category: Sauer, S.]]	+	[[Category: Sauer, S]]
-	[[Category: Schroeder, F C.]]	+	[[Category: Schroeder, F C]]
-	[[Category: Weidner, C.]]	+	[[Category: Weidner, C]]
	[[Category: Agonist]]		[[Category: Agonist]]
	[[Category: Diabetes]]		[[Category: Diabetes]]
	[[Category: Insulin resistance]]		[[Category: Insulin resistance]]
	[[Category: Receptor]]		[[Category: Receptor]]

OCA at 07:31, 5 February 2014

OCA — Wed, 05 Feb 2014 07:31:26 GMT

←Older revision		Revision as of 07:31, 5 February 2014
Line 1:		Line 1:
	{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}		{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}
	===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===		===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===
		+	{{ABSTRACT_PUBMED_23286787}}

	==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==
-	[[4a4w]] 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=4A4W OCA].	+	[[4a4w]] 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=4A4W OCA].

	==Reference==		==Reference==
-	<references group="xtra"/><references/>	+	<ref group="xtra">PMID:023286787</ref><references group="xtra"/><references/>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Buessow, K.]]		[[Category: Buessow, K.]]
-	[[Category: Groot, J C.De.]]	+	[[Category: Groot, J C.de.]]
	[[Category: Kawamoto, K.]]		[[Category: Kawamoto, K.]]
	[[Category: Krausze, J.]]		[[Category: Krausze, J.]]

OCA at 17:33, 24 March 2013

OCA — Sun, 24 Mar 2013 17:33:44 GMT

←Older revision		Revision as of 17:33, 24 March 2013
Line 1:		Line 1:
-	[[Image:4a4w.jpg\|left\|200px]]
-
	{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}		{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}
-
	===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===		===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===

		+	==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==
	[[4a4w]] 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=4A4W OCA].		[[4a4w]] 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=4A4W OCA].
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Buessow, K.]]		[[Category: Buessow, K.]]

OCA at 06:22, 3 October 2012

OCA — Wed, 03 Oct 2012 06:22:26 GMT

←Older revision		Revision as of 06:22, 3 October 2012
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:4a4w.jpg\|left\|200px]]

-	~~The entry~~ 4a4w ~~is ON HOLD~~ ~~until Paper Publication~~	+	{{STRUCTURE_4a4w\| PDB=4a4w \| SCENE= }}

-	~~Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K.~~	+	===Ligand binding domain of human PPAR gamma in complex with amorfrutin B===

-	~~Description: Ligand binding domain of human PPAR gamma in complex~~ with ~~amorfrutin B~~	+
		+	==About this Structure==
		+	[[4a4w]] 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=4A4W OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Buessow, K.]]
		+	[[Category: Groot, J C.De.]]
		+	[[Category: Kawamoto, K.]]
		+	[[Category: Krausze, J.]]
		+	[[Category: Sauer, S.]]
		+	[[Category: Schroeder, F C.]]
		+	[[Category: Weidner, C.]]
		+	[[Category: Agonist]]
		+	[[Category: Diabetes]]
		+	[[Category: Insulin resistance]]
		+	[[Category: Receptor]]

OCA at 11:23, 9 November 2011

OCA — Wed, 09 Nov 2011 11:23:17 GMT

←Older revision		Revision as of 11:23, 9 November 2011
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 4a4w is ON HOLD	+	The entry 4a4w is ON HOLD until Paper Publication

	Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K.		Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K.

	Description: Ligand binding domain of human PPAR gamma in complex with amorfrutin B		Description: Ligand binding domain of human PPAR gamma in complex with amorfrutin B

OCA: Protected "4a4w" [edit=sysop:move=sysop]

OCA — Sun, 30 Oct 2011 09:03:01 GMT

Protected "4a4w" [edit=sysop:move=sysop]

←Older revision

Revision as of 09:03, 30 October 2011

OCA: New page: '''Unreleased structure''' The entry 4a4w is ON HOLD Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K. Description: Ligand binding domain of human...

OCA — Sun, 30 Oct 2011 09:03:00 GMT

New page: '''Unreleased structure''' The entry 4a4w is ON HOLD Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K. Description: Ligand binding domain of human...

New page

'''Unreleased structure'''

The entry 4a4w is ON HOLD

Authors: de Groot, J.C., Weidner, C., Krausze, J., Quedenau, C., Sauer, S., Buessow, K.

Description: Ligand binding domain of human PPAR gamma in complex with amorfrutin B