6cvp: Difference between revisions
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<StructureSection load='6cvp' size='340' side='right'caption='[[6cvp]], [[Resolution|resolution]] 2.00Å' scene=''> | <StructureSection load='6cvp' size='340' side='right'caption='[[6cvp]], [[Resolution|resolution]] 2.00Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[6cvp]] is a 6 chain structure with sequence from [ | <table><tr><td colspan='2'>[[6cvp]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6CVP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6CVP FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.999Å</td></tr> | ||
<tr id=' | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=AMP:ADENOSINE+MONOPHOSPHATE'>AMP</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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=6cvp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6cvp OCA], [https://pdbe.org/6cvp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6cvp RCSB], [https://www.ebi.ac.uk/pdbsum/6cvp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6cvp ProSAT]</span></td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | |||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [https://www.uniprot.org/uniprot/APTX_HUMAN APTX_HUMAN] Defects in APTX are the cause of ataxia-oculomotor apraxia syndrome (AOA) [MIM:[https://omim.org/entry/208920 208920]. AOA is an autosomal recessive syndrome characterized by early-onset cerebellar ataxia, oculomotor apraxia, early areflexia and late peripheral neuropathy.<ref>PMID:11586299</ref> <ref>PMID:11586300</ref> <ref>PMID:12196655</ref> <ref>PMID:12629250</ref> <ref>PMID:14506070</ref> <ref>PMID:15852392</ref> <ref>PMID:15699391</ref> | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/APTX_HUMAN APTX_HUMAN] DNA-binding protein involved in single-strand DNA break repair, double-strand DNA break repair and base excision repair. Resolves abortive DNA ligation intermediates formed either at base excision sites, or when DNA ligases attempt to repair non-ligatable breaks induced by reactive oxygen species. Catalyzes the release of adenylate groups covalently linked to 5'-phosphate termini, resulting in the production of 5'-phosphate termini that can be efficiently rejoined. Also able to hydrolyze adenosine 5'-monophosphoramidate (AMP-NH(2)) and diadenosine tetraphosphate (AppppA), but with lower catalytic activity.<ref>PMID:14755728</ref> <ref>PMID:15044383</ref> <ref>PMID:16547001</ref> <ref>PMID:16964241</ref> <ref>PMID:17276982</ref> | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Schellenberg | [[Category: Schellenberg MJ]] | ||
[[Category: Tumbale | [[Category: Tumbale PS]] | ||
[[Category: Williams | [[Category: Williams RS]] | ||