5e69: Difference between revisions

Line 1:

~~'''Unreleased structure'''~~

~~The~~ entry ~~5e69~~ is ~~ON HOLD~~ ~~until Feb 05 2018~~

==Glucocorticoid receptor DNA binding domain - IL8 NF-kB response element complex==

~~Authors~~:

== Structural highlights ==

<table><tr><td colspan='2'>[[5e69]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E69 OCA]. For a guided tour on the structure components use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E69 FirstGlance].

~~Description~~:

</td></tr><tr id='ligand'><td class="sblockLbl">[[Ligand|Ligands:]]</td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>

[[Category: ~~Unreleased Structures~~]]

<tr id='resources'><td class="sblockLbl">Resources:</td><td class="sblockDat">[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5e69 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e69 OCA], [http://pdbe.org/5e69 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e69 RCSB], [http://www.ebi.ac.uk/pdbsum/5e69 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e69 ProSAT]</td></tr>

</table>

== Disease ==

[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[http://omim.org/entry/138040 138040]]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref> <ref>PMID:1704018</ref> <ref>PMID:7683692</ref> <ref>PMID:11589680</ref> <ref>PMID:11701741</ref>

== Function ==

[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>

== References ==

__TOC__

</StructureSection>

[[Category: Herbst, A G]]

[[Category: Hudson, W H]]

[[Category: Ortlund, E A]]

[[Category: Rye, E A]]

[[Category: Dna binding protein-dna complex]]

[[Category: Dna binding protein]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 5e69 is ON HOLD  until Feb 05 2018
+==Glucocorticoid receptor DNA binding domain - IL8 NF-kB response element complex==
+<StructureSection load='5e69' size='340' side='right' caption='[[5e69]], [[Resolution|resolution]] 1.85&Aring;' scene=''>
-Authors:
+== Structural highlights ==
+<table><tr><td colspan='2'>[[5e69]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5E69 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5E69 FirstGlance]. <br>
-Description:
+</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-[[Category: Unreleased Structures]]
+<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[5e6a|5e6a]], [[5e6b|5e6b]], [[5e6c|5e6c]], [[5e6d|5e6d]]</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=5e69 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5e69 OCA], [http://pdbe.org/5e69 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5e69 RCSB], [http://www.ebi.ac.uk/pdbsum/5e69 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5e69 ProSAT]</span></td></tr>
+</table>
+== Disease ==
+[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[http://omim.org/entry/138040 138040]]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref> <ref>PMID:1704018</ref> <ref>PMID:7683692</ref> <ref>PMID:11589680</ref> <ref>PMID:11701741</ref>
+== Function ==
+[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref>
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Herbst, A G]]
+[[Category: Hudson, W H]]
+[[Category: Ortlund, E A]]
+[[Category: Rye, E A]]
+[[Category: Dna binding protein-dna complex]]
+[[Category: Dna binding protein]]