4uda: Difference between revisions
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''' | ==MR in complex with dexamethasone== | ||
<StructureSection load='4uda' size='340' side='right' caption='[[4uda]], [[Resolution|resolution]] 2.03Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4uda]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4UDA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4UDA FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=DEX:DEXAMETHASONE'>DEX</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr> | |||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4udb|4udb]], [[4udc|4udc]], [[4udd|4udd]]</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> | |||
[[Category: | <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=4uda FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4uda OCA], [http://pdbe.org/4uda PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4uda RCSB], [http://www.ebi.ac.uk/pdbsum/4uda PDBsum]</span></td></tr> | ||
</table> | |||
== 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> [[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/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> [[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> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Histone acetyltransferase]] | |||
[[Category: Aagaard, A]] | [[Category: Aagaard, A]] | ||
[[Category: Backstrom, S]] | [[Category: Backstrom, S]] | ||
[[Category: Bjursell, M]] | [[Category: Bjursell, M]] | ||
[[Category: | [[Category: Bodin, C]] | ||
[[Category: Cavallin, A]] | [[Category: Cavallin, A]] | ||
[[Category: Edman, K]] | |||
[[Category: Grebner, C]] | [[Category: Grebner, C]] | ||
[[Category: Guallar, V]] | [[Category: Guallar, V]] | ||
[[Category: Hogner, A]] | [[Category: Hogner, A]] | ||
[[Category: Hussein, A]] | |||
[[Category: Jellesmark-Jensen, T]] | |||
[[Category: Karlsson, U]] | |||
[[Category: Lecina, D]] | |||
[[Category: Lepisto, M]] | |||
[[Category: Nilsson, E]] | |||
[[Category: Takahashi, R]] | |||
[[Category: Wissler, L]] | |||
[[Category: Ligand complex]] | |||
[[Category: Nuclear hormone receptor]] | |||
[[Category: Peptide complex]] | |||
[[Category: Signaling protein]] | |||