3wmh: Difference between revisions
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==Human | |||
==Human PPAR gamma ligand binding domain in complex with a gammma selective synthetic partial agonist MEKT75== | |||
<StructureSection load='3wmh' size='340' side='right' caption='[[3wmh]], [[Resolution|resolution]] 2.10Å' scene=''> | <StructureSection load='3wmh' size='340' side='right' caption='[[3wmh]], [[Resolution|resolution]] 2.10Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=JJA:N-(PHENYLSULFONYL)-4-PROPOXY-3-({[4-(PYRIMIDIN-2-YL)BENZOYL]AMINO}METHYL)BENZAMIDE'>JJA</scene></td></tr> | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=JJA:N-(PHENYLSULFONYL)-4-PROPOXY-3-({[4-(PYRIMIDIN-2-YL)BENZOYL]AMINO}METHYL)BENZAMIDE'>JJA</scene></td></tr> | ||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3vso|3vso]], [[3vsp|3vsp]]</td></tr> | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3vso|3vso]], [[3vsp|3vsp]]</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=3wmh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3wmh OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3wmh RCSB], [http://www.ebi.ac.uk/pdbsum/3wmh 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=3wmh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3wmh OCA], [http://pdbe.org/3wmh PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3wmh RCSB], [http://www.ebi.ac.uk/pdbsum/3wmh PDBsum]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == |
Revision as of 10:08, 2 March 2016
Human PPAR gamma ligand binding domain in complex with a gammma selective synthetic partial agonist MEKT75Human PPAR gamma ligand binding domain in complex with a gammma selective synthetic partial agonist MEKT75
Structural highlights
Disease[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: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.[1] Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM: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.[2] [3] Genetic variations in PPARG can be associated with susceptibility to glioma type 1 (GLM1) [MIM: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[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.[4] [5] [6] References
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