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'''Unreleased structure'''


The entry 8dnh is ON HOLD  until Paper Publication
==Cryo-EM structure of nonmuscle beta-actin==
<StructureSection load='8dnh' size='340' side='right'caption='[[8dnh]], [[Resolution|resolution]] 2.99&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[8dnh]] is a 4 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=8DNH OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8DNH FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ACE:ACETYL+GROUP'>ACE</scene>, <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></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=8dnh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8dnh OCA], [https://pdbe.org/8dnh PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8dnh RCSB], [https://www.ebi.ac.uk/pdbsum/8dnh PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8dnh 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.
<div style="background-color:#fffaf0;">
== Publication Abstract from PubMed ==
Actin isoforms organize into distinct networks that are essential for the normal function of eukaryotic cells. Despite a high level of sequence and structure conservation, subtle differences in their design principles determine the interaction with myosin motors and actin-binding proteins. Therefore, identifying how the structure of actin isoforms relates to function is important for our understanding of normal cytoskeletal physiology. Here, we report the high-resolution structures of filamentous skeletal muscle alpha-actin (3.37 A), cardiac muscle alpha-actin (3.07 A), ss-actin (2.99 A), and gamma-actin (3.38 A) in the Mg(2+).ADP state with their native post-translational modifications. The structures revealed isoform-specific conformations of the N-terminus that shift closer to the filament surface upon myosin binding, thereby establishing isoform-specific interfaces. Collectively, the structures of single-isotype, post-translationally modified bare skeletal muscle alpha-actin, cardiac muscle alpha-actin, ss-actin, and gamma-actin reveal general principles, similarities, and differences between isoforms. They complement the repertoire of known actin structures and allow for a comprehensive understanding of in vitro and in vivo functions of actin isoforms.


Authors: Arora, A.S., Huang, H.L., Heissler, S.M., Chinthalapudi, K.
Structural insights into actin isoforms.,Arora AS, Huang HL, Singh R, Narui Y, Suchenko A, Hatano T, Heissler SM, Balasubramanian MK, Chinthalapudi K Elife. 2023 Feb 15;12:e82015. doi: 10.7554/eLife.82015. PMID:36790143<ref>PMID:36790143</ref>


Description: Cryo-EM structure of nonmuscle beta-actin
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
[[Category: Unreleased Structures]]
</div>
[[Category: Heissler, S.M]]
<div class="pdbe-citations 8dnh" style="background-color:#fffaf0;"></div>
[[Category: Huang, H.L]]
== References ==
[[Category: Chinthalapudi, K]]
<references/>
[[Category: Arora, A.S]]
__TOC__
</StructureSection>
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Arora AS]]
[[Category: Chinthalapudi K]]
[[Category: Heissler SM]]
[[Category: Huang HL]]
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