7u16: Difference between revisions
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==TMEM106B(120-254) protofilament from frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) type A (all cases combined).== | |||
<StructureSection load='7u16' size='340' side='right'caption='[[7u16]], [[Resolution|resolution]] 2.70Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7U16 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7U16 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]] 2.7Å</td></tr> | |||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</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=7u16 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7u16 OCA], [https://pdbe.org/7u16 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7u16 RCSB], [https://www.ebi.ac.uk/pdbsum/7u16 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7u16 ProSAT]</span></td></tr> | |||
</table> | |||
<div style="background-color:#fffaf0;"> | |||
== Publication Abstract from PubMed == | |||
Misfolding and aggregation of disease-specific proteins, resulting in the formation of filamentous cellular inclusions, is a hallmark of neurodegenerative disease with characteristic filament structures, or conformers, defining each proteinopathy. Here we show that a previously unsolved amyloid fibril composed of a 135 amino acid C-terminal fragment of TMEM106B is a common finding in distinct human neurodegenerative diseases, including cases characterized by abnormal aggregation of TDP-43, tau, or alpha-synuclein protein. A combination of cryoelectron microscopy and mass spectrometry was used to solve the structures of TMEM106B fibrils at a resolution of 2.7 A from postmortem human brain tissue afflicted with frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP, n = 8), progressive supranuclear palsy (PSP, n = 2), or dementia with Lewy bodies (DLB, n = 1). The commonality of abundant amyloid fibrils composed of TMEM106B, a lysosomal/endosomal protein, to a broad range of debilitating human disorders indicates a shared fibrillization pathway that may initiate or accelerate neurodegeneration. | |||
, PMID:35247328<ref>PMID:35247328</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
[[Category: | </div> | ||
<div class="pdbe-citations 7u16" style="background-color:#fffaf0;"></div> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Large Structures]] | |||
[[Category: Arakhamia T]] | |||
[[Category: Carlomagno Y]] | |||
[[Category: Chang A]] | |||
[[Category: Cook CN]] | |||
[[Category: DeMarco ML]] | |||
[[Category: DeTure M]] | |||
[[Category: Dhingra S]] | |||
[[Category: Dickson D]] | |||
[[Category: Fitzpatrick AWP]] | |||
[[Category: Forgrave LM]] | |||
[[Category: Heeman B]] | |||
[[Category: Lee C]] | |||
[[Category: Mackenzie IRA]] | |||
[[Category: Perneel J]] | |||
[[Category: Petrucelli L]] | |||
[[Category: Rademakers R]] | |||
[[Category: Simjanoska M]] | |||
[[Category: Stowell MHB]] | |||
[[Category: Thierry M]] | |||
[[Category: Wang C]] | |||
[[Category: Wang J]] | |||
[[Category: Xiang X]] | |||
[[Category: Zhang G]] | |||