6es7: Difference between revisions

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'''Unreleased structure'''


The entry 6es7 is ON HOLD
==Structure and dynamics conspire in the evolution of affinity between intrinsically disordered proteins==
 
<StructureSection load='6es7' size='340' side='right' caption='[[6es7]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
Authors: Chi, N.C.
== Structural highlights ==
 
<table><tr><td colspan='2'>[[6es7]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6ES7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6ES7 FirstGlance]. <br>
Description: Structure and dynamics conspire in the evolution of affinity between intrinsically disordered proteins
</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: 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=6es7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6es7 OCA], [http://pdbe.org/6es7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6es7 RCSB], [http://www.ebi.ac.uk/pdbsum/6es7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6es7 ProSAT]</span></td></tr>
[[Category: Chi, N.C]]
</table>
== Disease ==
[[http://www.uniprot.org/uniprot/CBP_HUMAN CBP_HUMAN]] Note=Chromosomal aberrations involving CREBBP may be a cause of acute myeloid leukemias. Translocation t(8;16)(p11;p13) with KAT6A; translocation t(11;16)(q23;p13.3) with MLL/HRX; translocation t(10;16)(q22;p13) with KAT6B. KAT6A-CREBBP may induce leukemia by inhibiting RUNX1-mediated transcription.  Defects in CREBBP are a cause of Rubinstein-Taybi syndrome type 1 (RSTS1) [MIM:[http://omim.org/entry/180849 180849]]. RSTS1 is an autosomal dominant disorder characterized by craniofacial abnormalities, broad thumbs, broad big toes, mental retardation and a propensity for development of malignancies.<ref>PMID:11331617</ref> <ref>PMID:12114483</ref> <ref>PMID:12566391</ref> <ref>PMID:15706485</ref> 
== Function ==
[[http://www.uniprot.org/uniprot/NCOA3_HUMAN NCOA3_HUMAN]] Nuclear receptor coactivator that directly binds nuclear receptors and stimulates the transcriptional activities in a hormone-dependent fashion. Plays a central role in creating a multisubunit coactivator complex, which probably acts via remodeling of chromatin. Involved in the coactivation of different nuclear receptors, such as for steroids (GR and ER), retinoids (RARs and RXRs), thyroid hormone (TRs), vitamin D3 (VDR) and prostanoids (PPARs). Displays histone acetyltransferase activity. Also involved in the coactivation of the NF-kappa-B pathway via its interaction with the NFKB1 subunit. Interacts with PSMB9. [[http://www.uniprot.org/uniprot/CBP_HUMAN CBP_HUMAN]] Acetylates histones, giving a specific tag for transcriptional activation. Also acetylates non-histone proteins, like NCOA3 and FOXO1. Binds specifically to phosphorylated CREB and enhances its transcriptional activity toward cAMP-responsive genes. Acts as a coactivator of ALX1 in the presence of EP300.<ref>PMID:9707565</ref> <ref>PMID:11154691</ref> <ref>PMID:12738767</ref> <ref>PMID:12929931</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Histone acetyltransferase]]
[[Category: Chi, N C]]
[[Category: Cid]]
[[Category: Complex]]
[[Category: Dna binding protein]]
[[Category: Idp]]
[[Category: Ncbd]]

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