4pf3: Difference between revisions

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==Mineralocorticoid receptor ligand-binding domain with compuond 37a==
==Mineralocorticoid receptor ligand-binding domain with compuond 37a==
<StructureSection load='4pf3' size='340' side='right' caption='[[4pf3]], [[Resolution|resolution]] 1.10&Aring;' scene=''>
<StructureSection load='4pf3' size='340' side='right'caption='[[4pf3]], [[Resolution|resolution]] 1.10&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[4pf3]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4PF3 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4PF3 FirstGlance]. <br>
<table><tr><td colspan='2'>[[4pf3]] is a 1 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=4PF3 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4PF3 FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=HFN:6-[1-(2,2-DIFLUORO-3-HYDROXYPROPYL)-5-(4-FLUOROPHENYL)-3-METHYL-1H-PYRAZOL-4-YL]-2H-1,4-BENZOXAZIN-3(4H)-ONE'>HFN</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]] 1.1&#8491;</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=4pf3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pf3 OCA], [http://pdbe.org/4pf3 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4pf3 RCSB], [http://www.ebi.ac.uk/pdbsum/4pf3 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4pf3 ProSAT]</span></td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=HFN:6-[1-(2,2-DIFLUORO-3-HYDROXYPROPYL)-5-(4-FLUOROPHENYL)-3-METHYL-1H-PYRAZOL-4-YL]-2H-1,4-BENZOXAZIN-3(4H)-ONE'>HFN</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=4pf3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pf3 OCA], [https://pdbe.org/4pf3 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4pf3 RCSB], [https://www.ebi.ac.uk/pdbsum/4pf3 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4pf3 ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/MCR_HUMAN MCR_HUMAN]] Defects in NR3C2 are a cause of pseudohypoaldosteronism 1, autosomal dominant (PHA1A) [MIM:[http://omim.org/entry/177735 177735]]. A salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. PHA1A is a mild form characterized by target organ defects confined to kidney. Patients may present with neonatal renal salt wasting with hyperkalaemic acidosis despite high aldosterone levels. These patients improve with age and usually become asymptomatic without treatment.<ref>PMID:9662404</ref> <ref>PMID:11134129</ref> <ref>PMID:12788847</ref> <ref>PMID:16954160</ref> <ref>PMID:16972228</ref>  Defects in NR3C2 are a cause of early-onset hypertension with severe exacerbation in pregnancy (EOHSEP) [MIM:[http://omim.org/entry/605115 605115]]. Inheritance is autosomal dominant. The disease is characterized by the onset of severe hypertension before the age of 20, and by suppression of aldosterone secretion.<ref>PMID:9662404</ref> <ref>PMID:15967794</ref> <ref>PMID:15908963</ref> <ref>PMID:10884226</ref>
[https://www.uniprot.org/uniprot/MCR_HUMAN MCR_HUMAN] Defects in NR3C2 are a cause of pseudohypoaldosteronism 1, autosomal dominant (PHA1A) [MIM:[https://omim.org/entry/177735 177735]. A salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. PHA1A is a mild form characterized by target organ defects confined to kidney. Patients may present with neonatal renal salt wasting with hyperkalaemic acidosis despite high aldosterone levels. These patients improve with age and usually become asymptomatic without treatment.<ref>PMID:9662404</ref> <ref>PMID:11134129</ref> <ref>PMID:12788847</ref> <ref>PMID:16954160</ref> <ref>PMID:16972228</ref>  Defects in NR3C2 are a cause of early-onset hypertension with severe exacerbation in pregnancy (EOHSEP) [MIM:[https://omim.org/entry/605115 605115]. Inheritance is autosomal dominant. The disease is characterized by the onset of severe hypertension before the age of 20, and by suppression of aldosterone secretion.<ref>PMID:9662404</ref> <ref>PMID:15967794</ref> <ref>PMID:15908963</ref> <ref>PMID:10884226</ref>  
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/MCR_HUMAN MCR_HUMAN]] Receptor for both mineralocorticoids (MC) such as aldosterone and glucocorticoids (GC) such as corticosterone or cortisol. Binds to mineralocorticoid response elements (MRE) and transactivates target genes. The effect of MC is to increase ion and water transport and thus raise extracellular fluid volume and blood pressure and lower potassium levels.<ref>PMID:3037703</ref>
[https://www.uniprot.org/uniprot/MCR_HUMAN MCR_HUMAN] Receptor for both mineralocorticoids (MC) such as aldosterone and glucocorticoids (GC) such as corticosterone or cortisol. Binds to mineralocorticoid response elements (MRE) and transactivates target genes. The effect of MC is to increase ion and water transport and thus raise extracellular fluid volume and blood pressure and lower potassium levels.<ref>PMID:3037703</ref>  
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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<div class="pdbe-citations 4pf3" style="background-color:#fffaf0;"></div>
==See Also==
*[[Mineralocorticoid receptor|Mineralocorticoid receptor]]
== References ==
== References ==
<references/>
<references/>
__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Habuka, N]]
[[Category: Homo sapiens]]
[[Category: Sogabe, S]]
[[Category: Large Structures]]
[[Category: Activating mutation]]
[[Category: Habuka N]]
[[Category: Hypertension]]
[[Category: Sogabe S]]
[[Category: Non-steroidal antagonist]]
[[Category: Nuclear receptor]]
[[Category: Transcription factor]]

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