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{{STRUCTURE_3kt9|  PDB=3kt9  |  SCENE=  }}
===Aprataxin FHA Domain===
{{ABSTRACT_PUBMED_20008512}}


==Disease==
==Aprataxin FHA Domain==
[[http://www.uniprot.org/uniprot/APTX_HUMAN APTX_HUMAN]] Defects in APTX are the cause of ataxia-oculomotor apraxia syndrome (AOA) [MIM:[http://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>  
<StructureSection load='3kt9' size='340' side='right'caption='[[3kt9]], [[Resolution|resolution]] 1.65&Aring;' scene=''>
 
== Structural highlights ==
==Function==
<table><tr><td colspan='2'>[[3kt9]] is a 1 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=3KT9 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3KT9 FirstGlance]. <br>
[[http://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>  
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.65&#8491;</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=3kt9 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3kt9 OCA], [https://pdbe.org/3kt9 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3kt9 RCSB], [https://www.ebi.ac.uk/pdbsum/3kt9 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3kt9 ProSAT]</span></td></tr>
==About this Structure==
</table>
[[3kt9]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KT9 OCA].  
== 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>  
==Reference==
== Function ==
<ref group="xtra">PMID:020008512</ref><references group="xtra"/><references/>
[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>  
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
  <jmolCheckbox>
    <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/kt/3kt9_consurf.spt"</scriptWhenChecked>
    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
    <text>to colour the structure by Evolutionary Conservation</text>
  </jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3kt9 ConSurf].
<div style="clear:both"></div>
== References ==
<references/>
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Cherry, A L.]]
[[Category: Large Structures]]
[[Category: Smerdon, S J.]]
[[Category: Cherry AL]]
[[Category: Amp hydrolase]]
[[Category: Smerdon SJ]]
[[Category: Beta sandwich]]
[[Category: Beta sheet]]
[[Category: Disease mutation]]
[[Category: Dna damage]]
[[Category: Dna repair]]
[[Category: Dna-binding]]
[[Category: Fha domain]]
[[Category: Hydrolase]]
[[Category: Metal-binding]]
[[Category: Neurodegeneration]]
[[Category: Nucleus]]
[[Category: Zinc-finger]]
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