4pkh
From Proteopedia
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<StructureSection load='4pkh' size='340' side='right'caption='[[4pkh]], [[Resolution|resolution]] 2.15Å' scene=''> | <StructureSection load='4pkh' size='340' side='right'caption='[[4pkh]], [[Resolution|resolution]] 2.15Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
- | <table><tr><td colspan='2'>[[4pkh]] is a 8 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[4pkh]] is a 8 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Oryctolagus_cuniculus Oryctolagus cuniculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4PKH OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4PKH FirstGlance]. <br> |
- | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene> | + | </td></tr><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=CA:CALCIUM+ION'>CA</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=4pkh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4pkh OCA], [https://pdbe.org/4pkh PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4pkh RCSB], [https://www.ebi.ac.uk/pdbsum/4pkh PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4pkh ProSAT]</span></td></tr> | |
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- | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | |
</table> | </table> | ||
- | == Disease == | ||
- | [[http://www.uniprot.org/uniprot/GELS_HUMAN GELS_HUMAN]] Defects in GSN are the cause of amyloidosis type 5 (AMYL5) [MIM:[http://omim.org/entry/105120 105120]]; also known as familial amyloidosis Finnish type. AMYL5 is a hereditary generalized amyloidosis due to gelsolin amyloid deposition. It is typically characterized by cranial neuropathy and lattice corneal dystrophy. Most patients have modest involvement of internal organs, but severe systemic disease can develop in some individuals causing peripheral polyneuropathy, amyloid cardiomyopathy, and nephrotic syndrome leading to renal failure.<ref>PMID:2157434</ref> <ref>PMID:2153578</ref> <ref>PMID:2176481</ref> <ref>PMID:1338910</ref> | ||
== Function == | == Function == | ||
- | [ | + | [https://www.uniprot.org/uniprot/ACTS_RABIT ACTS_RABIT] 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;"> | <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: Oryctolagus cuniculus]] | [[Category: Oryctolagus cuniculus]] | ||
- | [[Category: Dominguez | + | [[Category: Dominguez R]] |
- | [[Category: Rao | + | [[Category: Rao JN]] |
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Revision as of 13:10, 1 February 2023
Complex of ADP-actin With the N-terminal Actin-Binding Domain of Tropomodulin
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