6khz
From Proteopedia
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| - | '''Unreleased structure''' | ||
| - | + | ==p62/SQSTM1 ZZ domain with Gly-peptide== | |
| + | <StructureSection load='6khz' size='340' side='right'caption='[[6khz]], [[Resolution|resolution]] 2.80Å' scene=''> | ||
| + | == Structural highlights == | ||
| + | <table><tr><td colspan='2'>[[6khz]] is a 4 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=6KHZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6KHZ FirstGlance]. <br> | ||
| + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.8Å</td></tr> | ||
| + | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ZN:ZINC+ION'>ZN</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=6khz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6khz OCA], [https://pdbe.org/6khz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6khz RCSB], [https://www.ebi.ac.uk/pdbsum/6khz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6khz ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
| + | [https://www.uniprot.org/uniprot/SQSTM_HUMAN SQSTM_HUMAN] Defects in SQSTM1 are a cause of Paget disease of bone (PDB) [MIM:[https://omim.org/entry/602080 602080]. PDB is a metabolic bone disease affecting the axial skeleton and characterized by focal areas of increased and disorganized bone turn-over due to activated osteoclasts. Manifestations of the disease include bone pain, deformity, pathological fractures, deafness, neurological complications and increased risk of osteosarcoma. PDB is a chronic disease affecting 2 to 3% of the population above the age of 40 years.<ref>PMID:19931284</ref> <ref>PMID:11992264</ref> <ref>PMID:12374763</ref> <ref>PMID:14584883</ref> <ref>PMID:15146436</ref> <ref>PMID:15207768</ref> <ref>PMID:15125799</ref> <ref>PMID:15176995</ref> Note=In a cell model for Huntington disease (HD), appears to form a shell surrounding aggregates of mutant HTT that may protect cells from apoptosis, possibly by recruiting autophagosomal components to the polyubiquitinylated protein aggregates.<ref>PMID:16286508</ref> | ||
| + | == Function == | ||
| + | [https://www.uniprot.org/uniprot/SQSTM_HUMAN SQSTM_HUMAN] Required both for the formation and autophagic degradation of polyubiquitin-containing bodies, called ALIS (aggresome-like induced structures). Links ALIS to the autophagic machinery via direct interaction with MAP1 LC3 family members. May regulate the activation of NFKB1 by TNF-alpha, nerve growth factor (NGF) and interleukin-1. May play a role in titin/TTN downstream signaling in muscle cells. May regulate signaling cascades through ubiquitination. Adapter that mediates the interaction between TRAF6 and CYLD (By similarity). May be involved in cell differentiation, apoptosis, immune response and regulation of K(+) channels.<ref>PMID:10356400</ref> <ref>PMID:10747026</ref> <ref>PMID:11244088</ref> <ref>PMID:12471037</ref> <ref>PMID:15340068</ref> <ref>PMID:16079148</ref> <ref>PMID:16286508</ref> <ref>PMID:15953362</ref> <ref>PMID:15911346</ref> <ref>PMID:15802564</ref> <ref>PMID:19931284</ref> | ||
| + | <div style="background-color:#fffaf0;"> | ||
| + | == Publication Abstract from PubMed == | ||
| + | The N-degron pathway, formerly the N-end rule pathway, is a protein degradation process that determines the half-life of proteins based on their N-terminal residues. In contrast to the well-established in vivo studies over decades, in vitro studies of this pathway, including biochemical characterization and high-resolution structures, are relatively limited. In this study, we have developed a unique fusion technique using microtubule-associated protein 1A/1B light chain 3B, a key marker protein of autophagy, to tag the N-terminus of the proteins involved in the N-degron pathway, which enables high yield of homogeneous target proteins with variable N-terminal residues for diverse biochemical studies including enzymatic and binding assays and substrate identification. Intriguingly, crystallization showed a markedly enhanced probability, even for the N-degron complexes. To validate our results, we determined the structures of select proteins in the N-degron pathway and compared them to the PDB-deposited proteins. Furthermore, several biochemical applications of this technique were introduced. Therefore, this technique can be used as a general tool for the in vitro study of the N-degron pathway. | ||
| - | + | Use of the LC3B-fusion technique for biochemical and structural studies of proteins involved in the N-degron pathway.,Kim L, Kwon DH, Heo J, Park MR, Song HK J Biol Chem. 2020 Jan 9. pii: RA119.010912. doi: 10.1074/jbc.RA119.010912. PMID:31919097<ref>PMID:31919097</ref> | |
| - | + | From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |
| - | [[Category: | + | </div> |
| - | [[Category: | + | <div class="pdbe-citations 6khz" style="background-color:#fffaf0;"></div> |
| - | [[Category: Kim | + | |
| - | [[Category: Song | + | ==See Also== |
| + | *[[Sequestosome|Sequestosome]] | ||
| + | == References == | ||
| + | <references/> | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
| + | [[Category: Homo sapiens]] | ||
| + | [[Category: Large Structures]] | ||
| + | [[Category: Kim L]] | ||
| + | [[Category: Kwon DH]] | ||
| + | [[Category: Song HK]] | ||
Current revision
p62/SQSTM1 ZZ domain with Gly-peptide
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