5xac: Difference between revisions
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<StructureSection load='5xac' size='340' side='right'caption='[[5xac]], [[Resolution|resolution]] 1.70Å' scene=''> | <StructureSection load='5xac' size='340' side='right'caption='[[5xac]], [[Resolution|resolution]] 1.70Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[5xac]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5XAC OCA]. For a <b>guided tour on the structure components</b> use [ | <table><tr><td colspan='2'>[[5xac]] 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=5XAC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5XAC FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.701Å</td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5xac FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5xac OCA], [https://pdbe.org/5xac PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5xac RCSB], [https://www.ebi.ac.uk/pdbsum/5xac PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5xac ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/MLP3B_HUMAN MLP3B_HUMAN] Involved in formation of autophagosomal vacuoles (autophagosomes). | ||
<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: Homo sapiens]] | |||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Kim | [[Category: Kim L]] | ||
[[Category: Kwon | [[Category: Kwon DH]] | ||
[[Category: Song | [[Category: Song HK]] | ||
Latest revision as of 10:58, 22 November 2023
CLIR - LC3BCLIR - LC3B
Structural highlights
FunctionMLP3B_HUMAN Involved in formation of autophagosomal vacuoles (autophagosomes). Publication Abstract from PubMedLC3-family member proteins play a critical role in autophagy, a cellular process responsible for the degradation of massive cellular components including intracellular pathogens. A variety of molecules involved in the autophagic pathway engage in specific interactions with a unique sequence motif referred to as the LIR (LC3-interacting region) motif. Although identification of conserved structural features of LIR motifs in complex with LC3-family members has established a canonical LIR motif, atypical conformations of LIR motifs have recently been revealed. Here, we determined the three-dimensional crystal structures of LC3B in complex with three different LIR motifs of RavZ from Legionella pneumophila, an intracellular pathogen that can manipulate the host autophagy system. The tandem LIR motifs located in the N-terminal region of RavZ adopt a novel beta-sheet conformation and thus provide specific ionic interactions with LC3B in addition to canonical hydrophobic plugged-in interactions. Consequently, these motifs possess higher binding affinity to LC3-family members than canonical LIR motifs, although the tandem repeats can only bind to one LC3 molecule. These findings broaden our understanding of the functional repertoire of LIR motifs in autophagy. A novel conformation of the LC3-interacting region motif revealed by the structure of a complex between LC3B and RavZ.,Kwon DH, Kim L, Kim BW, Kim JH, Roh KH, Choi EJ, Song HK Biochem Biophys Res Commun. 2017 Aug 26;490(3):1093-1099. doi:, 10.1016/j.bbrc.2017.06.173. Epub 2017 Jun 29. PMID:28668392[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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