9qew
From Proteopedia
(Difference between revisions)
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- | '''Unreleased structure''' | ||
- | + | ==Cryo-EM structure of the undecorated actin filament in the ADP-Pi state.== | |
- | + | <StructureSection load='9qew' size='340' side='right'caption='[[9qew]], [[Resolution|resolution]] 2.18Å' scene=''> | |
- | + | == Structural highlights == | |
- | + | <table><tr><td colspan='2'>[[9qew]] is a 5 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=9QEW OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9QEW 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]] 2.18Å</td></tr> | |
- | [[Category: | + | <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=HIC:4-METHYL-HISTIDINE'>HIC</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=PO4:PHOSPHATE+ION'>PO4</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=9qew FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9qew OCA], [https://pdbe.org/9qew PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9qew RCSB], [https://www.ebi.ac.uk/pdbsum/9qew PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9qew ProSAT]</span></td></tr> | ||
+ | </table> | ||
+ | == Disease == | ||
+ | [https://www.uniprot.org/uniprot/ACTB_HUMAN ACTB_HUMAN] Defects in ACTB are a cause of dystonia juvenile-onset (DYTJ) [MIM:[https://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:[https://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> | ||
+ | == Function == | ||
+ | [https://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. | ||
+ | == References == | ||
+ | <references/> | ||
+ | __TOC__ | ||
+ | </StructureSection> | ||
+ | [[Category: Homo sapiens]] | ||
+ | [[Category: Large Structures]] | ||
+ | [[Category: Bieling P]] | ||
+ | [[Category: Boiero Sanders M]] | ||
+ | [[Category: Hofnagel O]] | ||
+ | [[Category: Oosterheert W]] | ||
+ | [[Category: Raunser S]] |
Current revision
Cryo-EM structure of the undecorated actin filament in the ADP-Pi state.
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