3g9e - Revision history

OCA at 15:37, 1 November 2023

OCA — Wed, 01 Nov 2023 15:37:27 GMT

←Older revision		Revision as of 15:37, 1 November 2023
Line 3:		Line 3:
	<StructureSection load='3g9e' size='340' side='right'caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='3g9e' size='340' side='right'caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3G9E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3G9E FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=RO7:(2S)~~-~~2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1~~,~~3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</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]] 2.3Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>~~[[~~Related_structure~~\|~~Related:~~]]~~</b></td><td class="sblockDat"><div style='overflow: auto~~; ~~max-height: 3em;'>[[3g8i\|3g8i]]</div>~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</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='activity'><td class~~="~~sblockLbl~~"><~~b>Activity:</b></td><td class~~=~~"sblockDat"><span class~~=~~'plainlinks'>[https~~:~~//en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number~~ [~~https://www.brenda~~-~~enzymes.info/php/result_flat.php4?ecno=~~2~~.3.~~1~~.48 2.~~3~~.1.48~~] </~~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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [https://pdbe.org/3g9e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [https://www.ebi.ac.uk/pdbsum/3g9e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3g9e 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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [https://pdbe.org/3g9e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [https://www.ebi.ac.uk/pdbsum/3g9e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3g9e 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/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.	+	[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/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<ref>PMID:9427757</ref> <ref>PMID:7481822</ref> <ref>PMID:9223431</ref> <ref>PMID:9296499</ref> <ref>PMID:9223281</ref> <ref>PMID:10449719</ref> <ref>PMID:12954634</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]]
Line 40:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Histone acetyltransferase]]~~	+	[[Category: Homo sapiens]]
-	~~[[Category: Human~~]]	+
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Benz, J]]	+	[[Category: Benz J]]
-	[[Category: Bernardeau, A]]	+	[[Category: Bernardeau A]]
-	[[Category: Binggeli, A]]	+	[[Category: Binggeli A]]
-	[[Category: Blum, D]]	+	[[Category: Blum D]]
-	[[Category: Boehringer, M]]	+	[[Category: Boehringer M]]
-	[[Category: Grether, U]]	+	[[Category: Grether U]]
-	[[Category: Gsell, B]]	+	[[Category: Gsell B]]
-	[[Category: Hilpert, H]]	+	[[Category: Hilpert H]]
-	[[Category: Kuhn, B]]	+	[[Category: Kuhn B]]
-	[[Category: Maerki~~, H P~~]]	+	[[Category: Maerki HP]]
-	[[Category: Meyer, M]]	+	[[Category: Meyer M]]
-	[[Category: Mohr, P]]	+	[[Category: Mohr P]]
-	[[Category: Puenterner, K]]	+	[[Category: Puenterner K]]
-	[[Category: Raab, S]]	+	[[Category: Raab S]]
-	[[Category: Ruf, A]]	+	[[Category: Ruf A]]
-	[[Category: Schlatter, D]]	+	[[Category: Schlatter D]]
-	[[Category: Stihle, M]]	+	[[Category: Stihle M]]
-	~~[[Category: Activator]]~~	+
-	~~[[Category: Acyltransferase]]~~	+
-	~~[[Category: Alternative splicing]]~~	+
-	~~[[Category: Chromosomal rearrangement]]~~	+
-	~~[[Category: Diabetes]]~~	+
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Dna-binding]]~~	+
-	~~[[Category: Metal-binding]]~~	+
-	~~[[Category: Nuclear receptor]]~~	+
-	~~[[Category: Nucleus]]~~	+
-	~~[[Category: Obesity]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Polymorphism]]~~	+
-	~~[[Category: Proto-oncogene]]~~	+
-	~~[[Category: Receptor]]~~	+
-	~~[[Category: Transcription]]~~	+
-	~~[[Category: Transcription factor]]~~	+
-	~~[[Category: Transcription regulation]]~~	+
-	~~[[Category: Transcription-transferase complex]]~~	+
-	~~[[Category: Transferase]]~~	+
-	~~[[Category: Ubl conjugation]]~~	+
-	~~[[Category: Zinc]]~~	+
-	~~[[Category: Zinc-finger~~]]	+

OCA at 07:59, 9 March 2022

OCA — Wed, 09 Mar 2022 07:59:06 GMT

←Older revision		Revision as of 07:59, 9 March 2022
Line 1:		Line 1:

	==Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes==		==Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes==
-	<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>	+	<StructureSection load='3g9e' size='340' side='right'caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3G9E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3G9E FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3g8i\|3g8i]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3g8i\|3g8i]]</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='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [~~http~~://pdbe.org/3g9e PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3g9e PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3g9e 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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [https://pdbe.org/3g9e PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [https://www.ebi.ac.uk/pdbsum/3g9e PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3g9e 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. [[~~http~~://www.uniprot.org/uniprot/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.	+	[[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/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.
	== 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/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<ref>PMID:9427757</ref> <ref>PMID:7481822</ref> <ref>PMID:9223431</ref> <ref>PMID:9296499</ref> <ref>PMID:9223281</ref> <ref>PMID:10449719</ref> <ref>PMID:12954634</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> [[https://www.uniprot.org/uniprot/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<ref>PMID:9427757</ref> <ref>PMID:7481822</ref> <ref>PMID:9223431</ref> <ref>PMID:9296499</ref> <ref>PMID:9223281</ref> <ref>PMID:10449719</ref> <ref>PMID:12954634</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 35:		Line 35:

	==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 42:		Line 42:
	[[Category: Histone acetyltransferase]]		[[Category: Histone acetyltransferase]]
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Benz, J]]		[[Category: Benz, J]]
	[[Category: Bernardeau, A]]		[[Category: Bernardeau, A]]

OCA at 05:31, 7 December 2018

OCA — Fri, 07 Dec 2018 05:31:16 GMT

←Older revision		Revision as of 05:31, 7 December 2018
Line 1:		Line 1:
		+
	==Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes==		==Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes==
	<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>
Line 7:		Line 8:
	<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 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [http://pdbe.org/3g9e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [http://www.ebi.ac.uk/pdbsum/3g9e 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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [http://pdbe.org/3g9e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [http://www.ebi.ac.uk/pdbsum/3g9e PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3g9e ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 17:		Line 18:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/g9/3g9e_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/g9/3g9e_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
Line 60:		Line 61:
	[[Category: Activator]]		[[Category: Activator]]
	[[Category: Acyltransferase]]		[[Category: Acyltransferase]]
		+	[[Category: Alternative splicing]]
		+	[[Category: Chromosomal rearrangement]]
	[[Category: Diabetes]]		[[Category: Diabetes]]
	[[Category: Diabetes mellitus]]		[[Category: Diabetes mellitus]]
Line 69:		Line 72:
	[[Category: Obesity]]		[[Category: Obesity]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
		+	[[Category: Polymorphism]]
	[[Category: Proto-oncogene]]		[[Category: Proto-oncogene]]
	[[Category: Receptor]]		[[Category: Receptor]]
Line 76:		Line 80:
	[[Category: Transcription-transferase complex]]		[[Category: Transcription-transferase complex]]
	[[Category: Transferase]]		[[Category: Transferase]]
		+	[[Category: Ubl conjugation]]
		+	[[Category: Zinc]]
	[[Category: Zinc-finger]]		[[Category: Zinc-finger]]

OCA at 07:39, 8 February 2016

OCA — Mon, 08 Feb 2016 07:39:08 GMT

←Older revision		Revision as of 07:39, 8 February 2016
Line 2:		Line 2:
	<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>		<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3G9E FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3G9E FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3g8i\|3g8i]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3g8i\|3g8i]]</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='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [http://www.ebi.ac.uk/pdbsum/3g9e 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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [http://pdbe.org/3g9e PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [http://www.ebi.ac.uk/pdbsum/3g9e PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 21:		Line 21:
	<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=3g9e ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 31:		Line 31:
	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 3g9e" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 39:		Line 40:
	</StructureSection>		</StructureSection>
	[[Category: Histone acetyltransferase]]		[[Category: Histone acetyltransferase]]
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Benz, J]]		[[Category: Benz, J]]
	[[Category: Bernardeau, A]]		[[Category: Bernardeau, A]]

OCA at 22:54, 3 January 2015

OCA — Sat, 03 Jan 2015 22:54:12 GMT

←Older revision		Revision as of 22:54, 3 January 2015
Line 1:		Line 1:
-	~~{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}~~	+	==Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes==
-	===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===	+	<StructureSection load='3g9e' size='340' side='right' caption='[[3g9e]], [[Resolution\|resolution]] 2.30Å' scene=''>
-	{~~{ABSTRACT_PUBMED_19349176}~~}	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3g9e]] 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=3G9E OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3G9E FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=RO7:(2S)-2-METHOXY-3-{4-[2-(5-METHYL-2-PHENYL-1,3-OXAZOL-4-YL)ETHOXY]-1-BENZOTHIOPHEN-7-YL}PROPANOIC+ACID'>RO7</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3g8i\|3g8i]]</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='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone_acetyltransferase Histone acetyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.3.1.48 2.3.1.48] </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=3g9e FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3g9e OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3g9e RCSB], [http://www.ebi.ac.uk/pdbsum/3g9e 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/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.
		+	== 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/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<ref>PMID:9427757</ref> <ref>PMID:7481822</ref> <ref>PMID:9223431</ref> <ref>PMID:9296499</ref> <ref>PMID:9223281</ref> <ref>PMID:10449719</ref> <ref>PMID:12954634</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/g9/3g9e_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 ==
		+	Design, synthesis, and SAR of novel alpha-alkoxy-beta-arylpropionic acids as potent and balanced PPARalphagamma coagonists are described. One representative thereof, Aleglitazar ((S)-2Aa), was chosen for clinical development. Its X-ray structure in complex with both receptors as well as its high efficacy in animal models of T2D and dyslipidemia are also presented.

-	~~==Disease==~~	+	Aleglitazar, a new, potent, and balanced dual PPARalpha/gamma agonist for the treatment of type II diabetes.,Benardeau A, Benz J, Binggeli A, Blum D, Boehringer M, Grether U, Hilpert H, Kuhn B, Marki HP, Meyer M, Puntener K, Raab S, Ruf A, Schlatter D, Mohr P Bioorg Med Chem Lett. 2009 May 1;19(9):2468-73. Epub 2009 Mar 14. PMID:19349176<ref>PMID:19349176</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. [[http://www.uniprot.org/uniprot/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.	+

-	~~==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> [[http://www.uniprot.org/uniprot/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the ~~transcriptional activities in a hormone-dependent fashion~~. ~~Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs)~~. ~~Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance~~ of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<~~ref~~>~~PMID:9427757~~</~~ref~~>~~<ref>PMID:7481822</ref><ref>PMID:9223431</ref><ref>PMID:9296499</ref><ref>PMID:9223281</ref><ref>PMID:10449719</ref><ref>PMID:12954634</ref>~~	+	</div>
-		+
-	~~==About this Structure==~~	+
-	[[3g9e]] 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=3G9E OCA].	+

	==See Also==		==See Also==
	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]		*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:019349176</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Histone acetyltransferase]]		[[Category: Histone acetyltransferase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Benz, J.]]	+	[[Category: Benz, J]]
-	[[Category: Bernardeau, A.]]	+	[[Category: Bernardeau, A]]
-	[[Category: Binggeli, A.]]	+	[[Category: Binggeli, A]]
-	[[Category: Blum, D.]]	+	[[Category: Blum, D]]
-	[[Category: Boehringer, M.]]	+	[[Category: Boehringer, M]]
-	[[Category: Grether, U.]]	+	[[Category: Grether, U]]
-	[[Category: Gsell, B.]]	+	[[Category: Gsell, B]]
-	[[Category: Hilpert, H.]]	+	[[Category: Hilpert, H]]
-	[[Category: Kuhn, B.]]	+	[[Category: Kuhn, B]]
-	[[Category: Maerki, H P.]]	+	[[Category: Maerki, H P]]
-	[[Category: Meyer, M.]]	+	[[Category: Meyer, M]]
-	[[Category: Mohr, P.]]	+	[[Category: Mohr, P]]
-	[[Category: Puenterner, K.]]	+	[[Category: Puenterner, K]]
-	[[Category: Raab, S.]]	+	[[Category: Raab, S]]
-	[[Category: Ruf, A.]]	+	[[Category: Ruf, A]]
-	[[Category: Schlatter, D.]]	+	[[Category: Schlatter, D]]
-	[[Category: Stihle, M.]]	+	[[Category: Stihle, M]]
	[[Category: Activator]]		[[Category: Activator]]
	[[Category: Acyltransferase]]		[[Category: Acyltransferase]]

OCA at 06:43, 25 March 2013

OCA — Mon, 25 Mar 2013 06:43:00 GMT

←Older revision		Revision as of 06:43, 25 March 2013
Line 1:		Line 1:
-	[[Image:3g9e.png\|left\|200px]]
-
	{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}		{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}
-
	===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===		===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===
		+	{{ABSTRACT_PUBMED_19349176}}

-	~~{{ABSTRACT_PUBMED_19349176}}~~	+	==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/NCOA1_HUMAN NCOA1_HUMAN]] Note=A chromosomal aberration involving NCOA1 is a cause of rhabdomyosarcoma. Translocation t(2;2)(q35;p23) with PAX3 generates the NCOA1-PAX3 oncogene consisting of the N-terminus part of PAX3 and the C-terminus part of NCOA1. The fusion protein acts as a transcriptional activator. Rhabdomyosarcoma is the most common soft tissue carcinoma in childhood, representing 5-8% of all malignancies in children.
		+
		+	==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/NCOA1_HUMAN NCOA1_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Involved in the coactivation of different nuclear receptors, such as for steroids (PGR, GR and ER), retinoids (RXRs), thyroid hormone (TRs) and prostanoids (PPARs). Also involved in coactivation mediated by STAT3, STAT5A, STAT5B and STAT6 transcription factors. Displays histone acetyltransferase activity toward H3 and H4; the relevance of such activity remains however unclear. Plays a central role in creating multisubunit coactivator complexes that act via remodeling of chromatin, and possibly acts by participating in both chromatin remodeling and recruitment of general transcription factors. Required with NCOA2 to control energy balance between white and brown adipose tissues. Required for mediating steroid hormone response. Isoform 2 has a higher thyroid hormone-dependent transactivation activity than isoform 1 and isoform 3.<ref>PMID:9427757</ref><ref>PMID:7481822</ref><ref>PMID:9223431</ref><ref>PMID:9296499</ref><ref>PMID:9223281</ref><ref>PMID:10449719</ref><ref>PMID:12954634</ref>

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

	==Reference==		==Reference==
-	<ref group="xtra">PMID:019349176</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019349176</ref><references group="xtra"/><references/>
	[[Category: Histone acetyltransferase]]		[[Category: Histone acetyltransferase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA at 09:25, 20 October 2012

OCA — Sat, 20 Oct 2012 09:25:31 GMT

←Older revision		Revision as of 09:25, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3g9e]] 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=3G9E OCA].	+	[[3g9e]] 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=3G9E OCA].

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

OCA: Protected "3g9e" [edit=sysop:move=sysop]

OCA — Wed, 25 Jul 2012 22:48:31 GMT

Protected "3g9e" [edit=sysop:move=sysop]

←Older revision

Revision as of 22:48, 25 July 2012

OCA at 22:48, 25 July 2012

OCA — Wed, 25 Jul 2012 22:48:28 GMT

←Older revision		Revision as of 22:48, 25 July 2012
Line 1:		Line 1:
-	~~{{Seed}}~~	+	[[Image:3g9e.png\|left\|200px]]
-	[[Image:3g9e.~~jpg~~\|left\|200px]]	+

-	<!--
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-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
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-	-->
	{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}		{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}

	===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===		===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_19349176}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 19349176 is the PubMed ID number.
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	{{ABSTRACT_PUBMED_19349176}}		{{ABSTRACT_PUBMED_19349176}}

	==About this Structure==		==About this Structure==
-	~~3G9E~~ is a 2 ~~chains~~ structure of ~~sequences~~ from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3G9E OCA].	+	[[3g9e]] 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=3G9E OCA].
		+
		+	==See Also==
		+	*[[Peroxisome Proliferator-Activated Receptors\|Peroxisome Proliferator-Activated Receptors]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~19349176~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019349176</ref><references group="xtra"/>
	[[Category: Histone acetyltransferase]]		[[Category: Histone acetyltransferase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
Line 45:		Line 36:
	[[Category: Activator]]		[[Category: Activator]]
	[[Category: Acyltransferase]]		[[Category: Acyltransferase]]
-	[[Category: Alternative splicing]]
-	[[Category: Chromosomal rearrangement]]
	[[Category: Diabetes]]		[[Category: Diabetes]]
	[[Category: Diabetes mellitus]]		[[Category: Diabetes mellitus]]
Line 56:		Line 45:
	[[Category: Obesity]]		[[Category: Obesity]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
-	[[Category: Polymorphism]]
	[[Category: Proto-oncogene]]		[[Category: Proto-oncogene]]
	[[Category: Receptor]]		[[Category: Receptor]]
Line 62:		Line 50:
	[[Category: Transcription factor]]		[[Category: Transcription factor]]
	[[Category: Transcription regulation]]		[[Category: Transcription regulation]]
-	[[Category: Transcription/transferase complex]]	+	[[Category: Transcription-transferase complex]]
	[[Category: Transferase]]		[[Category: Transferase]]
-	[[Category: Ubl conjugation]]
-	[[Category: Zinc]]
	[[Category: Zinc-finger]]		[[Category: Zinc-finger]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Jun 4 07:25:48 2009''

OCA at 04:25, 4 June 2009

OCA — Thu, 04 Jun 2009 04:25:50 GMT

←Older revision		Revision as of 04:25, 4 June 2009
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	{{Seed}}
		+	[[Image:3g9e.jpg\|left\|200px]]

-	The ~~entry 3g9e~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3g9e", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_3g9e\| PDB=3g9e \| SCENE= }}

-	~~Authors: Benardeau, A~~.	+	===Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes===

-	Description: Aleglitaar. a new. potent, and balanced dual ppara/g agonist for the treatment of type II diabetes

-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on ~~Wed Mar 25 12~~:13:48 2009''	+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_19349176}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 19349176 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_19349176}}
		+
		+	==About this Structure==
		+	3G9E is a 2 chains structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3G9E OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:19349176</ref><references group="xtra"/>
		+	[[Category: Histone acetyltransferase]]
		+	[[Category: Homo sapiens]]
		+	[[Category: Benz, J.]]
		+	[[Category: Bernardeau, A.]]
		+	[[Category: Binggeli, A.]]
		+	[[Category: Blum, D.]]
		+	[[Category: Boehringer, M.]]
		+	[[Category: Grether, U.]]
		+	[[Category: Gsell, B.]]
		+	[[Category: Hilpert, H.]]
		+	[[Category: Kuhn, B.]]
		+	[[Category: Maerki, H P.]]
		+	[[Category: Meyer, M.]]
		+	[[Category: Mohr, P.]]
		+	[[Category: Puenterner, K.]]
		+	[[Category: Raab, S.]]
		+	[[Category: Ruf, A.]]
		+	[[Category: Schlatter, D.]]
		+	[[Category: Stihle, M.]]
		+	[[Category: Activator]]
		+	[[Category: Acyltransferase]]
		+	[[Category: Alternative splicing]]
		+	[[Category: Chromosomal rearrangement]]
		+	[[Category: Diabetes]]
		+	[[Category: Diabetes mellitus]]
		+	[[Category: Disease mutation]]
		+	[[Category: Dna-binding]]
		+	[[Category: Metal-binding]]
		+	[[Category: Nuclear receptor]]
		+	[[Category: Nucleus]]
		+	[[Category: Obesity]]
		+	[[Category: Phosphoprotein]]
		+	[[Category: Polymorphism]]
		+	[[Category: Proto-oncogene]]
		+	[[Category: Receptor]]
		+	[[Category: Transcription]]
		+	[[Category: Transcription factor]]
		+	[[Category: Transcription regulation]]
		+	[[Category: Transcription/transferase complex]]
		+	[[Category: Transferase]]
		+	[[Category: Ubl conjugation]]
		+	[[Category: Zinc]]
		+	[[Category: Zinc-finger]]
		+
		+	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Jun 4 07:25:48 2009''