4udd: Difference between revisions

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'''Unreleased structure'''
==GR in complex with desisobutyrylciclesonide==
 
<StructureSection load='4udd' size='340' side='right' caption='[[4udd]], [[Resolution|resolution]] 1.80&Aring;' scene=''>
The entry 4udd is ON HOLD  until Paper Publication
== Structural highlights ==
 
<table><tr><td colspan='2'>[[4udd]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4UDD OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4UDD FirstGlance]. <br>
Authors: EDMAN, K., HOGNER, A., HUSSEIN, A., BJURSELL, M., AAGAARD, A., BACKSTROM, S., BODIN, C., WISSLER, L., JELLESMARK-JENSEN, T., CAVALLIN, A., KARLSSON, U., NILSSON, E., LECINA, D., TAKAHASHI, R., GREBNER, C., LEPISTO, M., GUALLAR, V.
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CPS:3-[(3-CHOLAMIDOPROPYL)DIMETHYLAMMONIO]-1-PROPANESULFONATE'>CPS</scene>, <scene name='pdbligand=CV7:DESISOBUYTYRYL+CICLESONIDE'>CV7</scene>, <scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>
 
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4uda|4uda]], [[4udb|4udb]], [[4udc|4udc]]</td></tr>
Description: GR in complex with desisobutyrylciclesonide
<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=4udd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4udd OCA], [http://pdbe.org/4udd PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4udd RCSB], [http://www.ebi.ac.uk/pdbsum/4udd PDBsum]</span></td></tr>
[[Category: Unreleased Structures]]
</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>  [[http://www.uniprot.org/uniprot/NCOA2_HUMAN NCOA2_HUMAN]] Note=Chromosomal aberrations involving NCOA2 may be a cause of acute myeloid leukemias. Inversion inv(8)(p11;q13) generates the KAT6A-NCOA2 oncogene, which consists of the N-terminal part of KAT6A and the C-terminal part of NCOA2/TIF2. KAT6A-NCOA2 binds to CREBBP and disrupts its function in transcription activation.
== 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>  [[http://www.uniprot.org/uniprot/NCOA2_HUMAN NCOA2_HUMAN]] Transcriptional coactivator for steroid receptors and nuclear receptors. Coactivator of the steroid binding domain (AF-2) but not of the modulating N-terminal domain (AF-1). Required with NCOA1 to control energy balance between white and brown adipose tissues.<ref>PMID:9430642</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Aagaard, A]]
[[Category: Aagaard, A]]
[[Category: Edman, K]]
[[Category: Karlsson, U]]
[[Category: Backstrom, S]]
[[Category: Backstrom, S]]
[[Category: Jellesmark-Jensen, T]]
[[Category: Lecina, D]]
[[Category: Wissler, L]]
[[Category: Takahashi, R]]
[[Category: Hussein, A]]
[[Category: Bjursell, M]]
[[Category: Bjursell, M]]
[[Category: Nilsson, E]]
[[Category: Bodin, C]]
[[Category: Cavallin, A]]
[[Category: Cavallin, A]]
[[Category: Edman, K]]
[[Category: Grebner, C]]
[[Category: Grebner, C]]
[[Category: Lepisto, M]]
[[Category: Bodin, 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]]