6ict

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'''Unreleased structure'''
 
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The entry 6ict is ON HOLD until Paper Publication
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==Structure of SETD3 bound to SAH and methylated actin==
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<StructureSection load='6ict' size='340' side='right' caption='[[6ict]], [[Resolution|resolution]] 1.95&Aring;' scene=''>
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Authors:
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== Structural highlights ==
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<table><tr><td colspan='2'>[[6ict]] is a 8 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6ICT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6ICT FirstGlance]. <br>
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Description:
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SAH:S-ADENOSYL-L-HOMOCYSTEINE'>SAH</scene></td></tr>
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[[Category: Unreleased Structures]]
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<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=HIC:4-METHYL-HISTIDINE'>HIC</scene></td></tr>
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<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Histone-lysine_N-methyltransferase Histone-lysine N-methyltransferase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.1.1.43 2.1.1.43] </span></td></tr>
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<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=6ict FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ict OCA], [http://pdbe.org/6ict PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6ict RCSB], [http://www.ebi.ac.uk/pdbsum/6ict PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6ict ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/ACTB_HUMAN ACTB_HUMAN]] Defects in ACTB are a cause of dystonia juvenile-onset (DYTJ) [MIM:[http://omim.org/entry/607371 607371]]. DYTJ is a form of dystonia with juvenile onset. Dystonia is defined by the presence of sustained involuntary muscle contraction, often leading to abnormal postures. DYTJ patients manifest progressive, generalized, dopa-unresponsive dystonia, developmental malformations and sensory hearing loss.<ref>PMID:16685646</ref> Defects in ACTB are the cause of Baraitser-Winter syndrome type 1 (BRWS1) [MIM:[http://omim.org/entry/243310 243310]]. A rare developmental disorder characterized by the combination of congenital ptosis, high-arched eyebrows, hypertelorism, ocular colobomata, and a brain malformation consisting of anterior-predominant lissencephaly. Other typical features include postnatal short stature and microcephaly, intellectual disability, seizures, and hearing loss.<ref>PMID:22366783</ref>
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== Function ==
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[[http://www.uniprot.org/uniprot/SETD3_HUMAN SETD3_HUMAN]] Histone methyltransferase that methylates 'Lys-36' of histone H3 (H3K36me). H3 'Lys-36' methylation represents a specific tag for epigenetic transcriptional activation (By similarity). [[http://www.uniprot.org/uniprot/ACTB_HUMAN ACTB_HUMAN]] Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Histone-lysine N-methyltransferase]]
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[[Category: Guo, Q]]
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[[Category: Liao, S]]
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[[Category: Structural genomic]]
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[[Category: Xu, C]]
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[[Category: Histidine methylatransferase]]
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[[Category: Protein binding]]
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[[Category: Sgc]]

Revision as of 15:25, 27 February 2019

Structure of SETD3 bound to SAH and methylated actin

6ict, resolution 1.95Å

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