1sol: Difference between revisions
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==A PIP2 AND F-ACTIN-BINDING SITE OF GELSOLIN, RESIDUE 150-169 (NMR, AVERAGED STRUCTURE)== | ==A PIP2 AND F-ACTIN-BINDING SITE OF GELSOLIN, RESIDUE 150-169 (NMR, AVERAGED STRUCTURE)== | ||
<StructureSection load='1sol' size='340' side='right' caption='[[1sol | <StructureSection load='1sol' size='340' side='right'caption='[[1sol]]' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[1sol]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1SOL OCA]. For a <b>guided tour on the structure components</b> use [ | <table><tr><td colspan='2'>[[1sol]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1SOL OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1SOL FirstGlance]. <br> | ||
</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=1sol FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1sol OCA], [https://pdbe.org/1sol PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1sol RCSB], [https://www.ebi.ac.uk/pdbsum/1sol PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1sol ProSAT]</span></td></tr> | |||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [https://www.uniprot.org/uniprot/GELS_HUMAN GELS_HUMAN] Defects in GSN are the cause of amyloidosis type 5 (AMYL5) [MIM:[https://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/GELS_HUMAN GELS_HUMAN] Calcium-regulated, actin-modulating protein that binds to the plus (or barbed) ends of actin monomers or filaments, preventing monomer exchange (end-blocking or capping). It can promote the assembly of monomers into filaments (nucleation) as well as sever filaments already formed. Plays a role in ciliogenesis.<ref>PMID:20393563</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: | [[Category: Large Structures]] | ||
[[Category: | [[Category: Braunlin WH]] | ||
[[Category: | [[Category: Janmey PA]] | ||
[[Category: | [[Category: Vegners R]] | ||
[[Category: Xian W]] | |||