6bqu: Difference between revisions

Line 1:

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

~~The entry 6bqu is ON HOLD until Paper Publication~~

==Human GR (418-507) in complex with monomeric DNA binding site==

~~Authors: Pufall, M.A.~~

== Structural highlights ==

<table><tr><td colspan='2'>[[6bqu]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6BQU OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6BQU FirstGlance]. <br>

~~Description:~~ Human GR (418-507) in complex with monomeric DNA binding site

</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='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=6bqu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6bqu OCA], [http://pdbe.org/6bqu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6bqu RCSB], [http://www.ebi.ac.uk/pdbsum/6bqu PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6bqu ProSAT]</span></td></tr>

[[Category: Pufall, M.A]]

</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: Pufall, M A]]

[[Category: Dna binding protein]]

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

[[Category: Glucocorticoid receptor monomeric binding site]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 6bqu is ON HOLD  until Paper Publication
+==Human GR (418-507) in complex with monomeric DNA binding site==
+<StructureSection load='6bqu' size='340' side='right' caption='[[6bqu]], [[Resolution|resolution]] 2.50&Aring;' scene=''>
-Authors: Pufall, M.A.
+== Structural highlights ==
+<table><tr><td colspan='2'>[[6bqu]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6BQU OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6BQU FirstGlance]. <br>
-Description: Human GR (418-507) in complex with monomeric DNA binding site
+</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='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=6bqu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6bqu OCA], [http://pdbe.org/6bqu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6bqu RCSB], [http://www.ebi.ac.uk/pdbsum/6bqu PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6bqu ProSAT]</span></td></tr>
-[[Category: Pufall, M.A]]
+</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: Pufall, M A]]
+[[Category: Dna binding protein]]
+[[Category: Dna binding protein-dna complex]]
+[[Category: Glucocorticoid receptor monomeric binding site]]