View source for 7u13


==TMEM106B(120-254) singlet amyloid fibril from frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) type A (case 4)==
<StructureSection load='7u13' size='340' side='right'caption='[[7u13]], [[Resolution|resolution]] 2.90&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7U13 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7U13 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]] 2.9&#8491;</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=7u13 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7u13 OCA], [https://pdbe.org/7u13 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7u13 RCSB], [https://www.ebi.ac.uk/pdbsum/7u13 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7u13 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&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
</div>
<div class="pdbe-citations 7u13" 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]]