2ab2: Difference between revisions

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-{{STRUCTURE_2ab2|  PDB=2ab2  |  SCENE=  }}
-===Mineralocorticoid Receptor Double Mutant with Bound Spironolactone===
-{{ABSTRACT_PUBMED_15967794}}
-==Disease==
+==Mineralocorticoid Receptor Double Mutant with Bound Spironolactone==
-[[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>
+<StructureSection load='2ab2' size='340' side='right'caption='[[2ab2]], [[Resolution|resolution]] 1.85&Aring;' scene=''>
+== Structural highlights ==
+<table><tr><td colspan='2'>[[2ab2]] 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=2AB2 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2AB2 FirstGlance]. <br>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.85&#8491;</td></tr>
+<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SNL:SPIRONOLACTONE'>SNL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</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=2ab2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2ab2 OCA], [https://pdbe.org/2ab2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2ab2 RCSB], [https://www.ebi.ac.uk/pdbsum/2ab2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2ab2 ProSAT]</span></td></tr>
+</table>
+== Disease ==
+[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 ==
+[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>
+== 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/ab/2ab2_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/main_output.php?pdb_ID=2ab2 ConSurf].
+<div style="clear:both"></div>
-==Function==
+==See Also==
-[[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>
+*[[Mineralocorticoid receptor|Mineralocorticoid receptor]]
+== References ==
-==About this Structure==
+<references/>
-[[2ab2]] 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=2AB2 OCA].
+__TOC__
+</StructureSection>
-==Reference==
-<ref group="xtra">PMID:015967794</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
-[[Category: Apolito, C J.]]
+[[Category: Large Structures]]
-[[Category: Bledsoe, R K.]]
+[[Category: Apolito CJ]]
-[[Category: Holt, J A.]]
+[[Category: Bledsoe RK]]
-[[Category: Lambert, M H.]]
+[[Category: Holt JA]]
-[[Category: Madauss, K P.]]
+[[Category: Lambert MH]]
-[[Category: Pearce, K H.]]
+[[Category: Madauss KP]]
-[[Category: Stanley, T B.]]
+[[Category: Pearce KH]]
-[[Category: Stewart, E L.]]
+[[Category: Stanley TB]]
-[[Category: Trump, R P.]]
+[[Category: Stewart EL]]
-[[Category: Williams, S P.]]
+[[Category: Trump RP]]
-[[Category: Willson, T M.]]
+[[Category: Williams SP]]
-[[Category: Hypertension]]
+[[Category: Willson TM]]
-[[Category: Mineralocorticoid receptor]]
-[[Category: Mr]]
-[[Category: Nuclear receptor]]
-[[Category: Spironolactone]]
-[[Category: Steroid receptor]]
-[[Category: Transcription]]