View source for 9jao


==The structure of SMARCAD1 bound to the hexasome in the presence of ADP-BeFx==
<StructureSection load='9jao' size='340' side='right'caption='[[9jao]], [[Resolution|resolution]] 3.10&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[9jao]] is a 10 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens], [https://en.wikipedia.org/wiki/Xenopus_laevis Xenopus laevis] and [https://en.wikipedia.org/wiki/Synthetic_construct Synthetic construct]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=9JAO OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9JAO FirstGlance]. <br>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.1&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=BEF:BERYLLIUM+TRIFLUORIDE+ION'>BEF</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9jao FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9jao OCA], [https://pdbe.org/9jao PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9jao RCSB], [https://www.ebi.ac.uk/pdbsum/9jao PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9jao ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/SMRCD_HUMAN SMRCD_HUMAN] Huriez syndrome;Isolated congenital adermatoglyphia;Absence of fingerprints-congenital milia syndrome. The disease is caused by mutations affecting the gene represented in this entry. Splice site mutations causing aberrant splicing of skin-specific isoform 3 are likely to exert a loss-of-function effect and are involved in ADERM.<ref>PMID:21820097</ref> <ref>PMID:24909267</ref>   The disease is caused by mutations affecting the gene represented in this entry. Splice site mutations causing aberrant splicing of skin-specific isoform 3 are likely to exert a loss-of-function effect and are involved in BSNS.<ref>PMID:24664640</ref> <ref>PMID:26932190</ref> 
== Function ==
[https://www.uniprot.org/uniprot/SMRCD_HUMAN SMRCD_HUMAN] DNA helicase that possesses intrinsic ATP-dependent nucleosome-remodeling activity and is both required for DNA repair and heterochromatin organization. Promotes DNA end resection of double-strand breaks (DSBs) following DNA damage: probably acts by weakening histone DNA interactions in nucleosomes flanking DSBs. Required for the restoration of heterochromatin organization after replication. Acts at replication sites to facilitate the maintenance of heterochromatin by directing H3 and H4 histones deacetylation, H3 'Lys-9' trimethylation (H3K9me3) and restoration of silencing.<ref>PMID:21549307</ref> <ref>PMID:22960744</ref> 
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Synthetic construct]]
[[Category: Xenopus laevis]]
[[Category: Chen KJ]]
[[Category: Chen ZC]]
[[Category: Hu PJ]]
[[Category: Sia YY]]
[[Category: Xia X]]