View source for 4oln


==Ancestral Steroid Receptor 1 in complex with estrogen response element DNA==
<StructureSection load='4oln' size='340' side='right'caption='[[4oln]], [[Resolution|resolution]] 1.70&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[4oln]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Synthetic_construct_sequences Synthetic construct sequences]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4OLN OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4OLN FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4ond|4ond]], [[4oor|4oor]]</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=4oln FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4oln OCA], [http://pdbe.org/4oln PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4oln RCSB], [http://www.ebi.ac.uk/pdbsum/4oln PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4oln ProSAT]</span></td></tr>
</table>
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== Publication Abstract from PubMed ==
Complex gene regulatory networks require transcription factors (TFs) to bind distinct DNA sequences. To understand how novel TF specificity evolves, we combined phylogenetic, biochemical, and biophysical approaches to interrogate how DNA recognition diversified in the steroid hormone receptor (SR) family. After duplication of the ancestral SR, three mutations in one copy radically weakened binding to the ancestral estrogen response element (ERE) and improved binding to a new set of DNA sequences (steroid response elements, SREs). They did so by establishing unfavorable interactions with ERE and abolishing unfavorable interactions with SRE; also required were numerous permissive substitutions, which nonspecifically improved cooperativity and affinity of DNA binding. Our findings indicate that negative determinants of binding play key roles in TFs' DNA selectivity and-with our prior work on the evolution of SR ligand specificity during the same interval-show how a specific new gene regulatory module evolved without interfering with the integrity of the ancestral module.

Evolution of DNA specificity in a transcription factor family produced a new gene regulatory module.,McKeown AN, Bridgham JT, Anderson DW, Murphy MN, Ortlund EA, Thornton JW Cell. 2014 Sep 25;159(1):58-68. doi: 10.1016/j.cell.2014.09.003. PMID:25259920<ref>PMID:25259920</ref>

From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Large Structures]]
[[Category: Synthetic construct sequences]]
[[Category: Murphy, M N]]
[[Category: Ortlund, E O]]
[[Category: Estrogen receptor]]
[[Category: Nuclear receptor zinc finger]]
[[Category: Steroid receptor dna binding]]
[[Category: Transcription factor]]
[[Category: Transcription-dna complex]]