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8b7d

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'''Unreleased structure'''
 
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The entry 8b7d is ON HOLD until Paper Publication
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==Luminal domain of TMEM106B==
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<StructureSection load='8b7d' size='340' side='right'caption='[[8b7d]], [[Resolution|resolution]] 2.59&Aring;' scene=''>
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Authors:
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== Structural highlights ==
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<table><tr><td colspan='2'>[[8b7d]] is a 1 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=8B7D OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8B7D FirstGlance]. <br>
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Description:
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.59&#8491;</td></tr>
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[[Category: Unreleased Structures]]
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<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>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8b7d FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8b7d OCA], [https://pdbe.org/8b7d PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8b7d RCSB], [https://www.ebi.ac.uk/pdbsum/8b7d PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8b7d ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/T106B_HUMAN T106B_HUMAN] Progressive non-fluent aphasia;Semantic dementia;Behavioral variant of frontotemporal dementia. The gene represented in this entry acts as a disease modifier. Risk alleles confer genetic susceptibility by increasing gene expression (PubMed:20154673, PubMed:21178100). Increased expression may be the result of down-regulation of microRNA miR-132 and miR-212, that repress TMEM106B expression (PubMed:22895706). Thr-185 is a risk allele associated with lower GRN protein levels and early age at onset in GRN UP-FTD mutation carriers: it presents slower protein degradation that leads to higher steady-state TMEM106B levels, leading to alterations in the intracellular versus extracellular partitioning of GRN (PubMed:23742080).<ref>PMID:20154673</ref> <ref>PMID:21178100</ref> <ref>PMID:22895706</ref> <ref>PMID:23742080</ref> The gene represented in this entry acts as a disease modifier. The disease may be caused by variants affecting the gene represented in this entry.
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== Function ==
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[https://www.uniprot.org/uniprot/T106B_HUMAN T106B_HUMAN] Involved in dendrite morphogenesis and maintenance by regulating lysosomal trafficking via its interaction with MAP6. May act by inhibiting retrograde transport of lysosomes along dendrites. Required for dendrite branching.<ref>PMID:23136129</ref> <ref>PMID:24357581</ref>
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Homo sapiens]]
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[[Category: Large Structures]]
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[[Category: Cherepanov P]]
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[[Category: Pye VE]]
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[[Category: Roustan C]]

Current revision

Luminal domain of TMEM106B

PDB ID 8b7d

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