6lpc: Difference between revisions
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<StructureSection load='6lpc' size='340' side='right'caption='[[6lpc]], [[Resolution|resolution]] 3.40Å' scene=''> | <StructureSection load='6lpc' size='340' side='right'caption='[[6lpc]], [[Resolution|resolution]] 3.40Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[6lpc]] is a 2 chain structure with sequence from [ | <table><tr><td colspan='2'>[[6lpc]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Rattus_norvegicus Rattus norvegicus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6LPC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6LPC 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]] 3.402Å</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=6lpc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6lpc OCA], [https://pdbe.org/6lpc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6lpc RCSB], [https://www.ebi.ac.uk/pdbsum/6lpc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6lpc ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/STXB1_RAT STXB1_RAT] May participate in the regulation of synaptic vesicle docking and fusion, possibly through interaction with GTP-binding proteins. Essential for neurotransmission and binds syntaxin, a component of the synaptic vesicle fusion machinery probably in a 1:1 ratio. Can interact with syntaxins 1, 2, and 3 but not syntaxin 4. May play a role in determining the specificity of intracellular fusion reactions. | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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</div> | </div> | ||
<div class="pdbe-citations 6lpc" style="background-color:#fffaf0;"></div> | <div class="pdbe-citations 6lpc" style="background-color:#fffaf0;"></div> | ||
==See Also== | |||
*[[Syntaxin-binding protein|Syntaxin-binding protein]] | |||
== References == | == References == | ||
<references/> | <references/> | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Gong | [[Category: Rattus norvegicus]] | ||
[[Category: Ma | [[Category: Gong JH]] | ||
[[Category: Wang | [[Category: Ma C]] | ||
[[Category: Wang | [[Category: Wang S]] | ||
[[Category: Xu | [[Category: Wang XP]] | ||
[[Category: Yang | [[Category: Xu YY]] | ||
[[Category: Yang | [[Category: Yang XF]] | ||
[[Category: Zhu | [[Category: Yang XY]] | ||
[[Category: Zhu L]] | |||
Latest revision as of 17:42, 29 November 2023
Crystal Structure of rat Munc18-1 with K332E/K333E mutationCrystal Structure of rat Munc18-1 with K332E/K333E mutation
Structural highlights
FunctionSTXB1_RAT May participate in the regulation of synaptic vesicle docking and fusion, possibly through interaction with GTP-binding proteins. Essential for neurotransmission and binds syntaxin, a component of the synaptic vesicle fusion machinery probably in a 1:1 ratio. Can interact with syntaxins 1, 2, and 3 but not syntaxin 4. May play a role in determining the specificity of intracellular fusion reactions. Publication Abstract from PubMedPriming of synaptic vesicles involves Munc13-catalyzed transition of the Munc18-1/syntaxin-1 complex to the SNARE complex in the presence of SNAP-25 and synaptobrevin-2; Munc13 drives opening of syntaxin-1 via the MUN domain while Munc18-1 primes SNARE assembly via domain 3a. However, the underlying mechanism remains unclear. In this study, we have identified a number of residues in domain 3a of Munc18-1 that are crucial for Munc13 and Munc18-1 actions in SNARE complex assembly and synaptic vesicle priming. Our results showed that two residues (Q301/K308) at the side of domain 3a mediate the interaction between the Munc18-1/syntaxin-1 complex and the MUN domain. This interaction enables the MUN domain to drive the opening of syntaxin-1 linker region, thereby leading to the extension of domain 3a and promoting synaptobrevin-2 binding. In addition, we identified two residues (K332/K333) at the bottom of domain 3a that mediate the interaction between Munc18-1 and the SNARE motif of syntaxin-1. This interaction ensures Munc18-1 to persistently associate with syntaxin-1 during the conformational change of syntaxin-1 from closed to open, which reinforces the role of Munc18-1 in templating SNARE assembly. Taken together, our data suggest a mechanism by which Munc13 activates the Munc18-1/syntaxin-1 complex and enables Munc18-1 to prime SNARE assembly. Munc13 activates the Munc18-1/syntaxin-1 complex and enables Munc18-1 to prime SNARE assembly.,Wang X, Gong J, Zhu L, Wang S, Yang X, Xu Y, Yang X, Ma C EMBO J. 2020 Jul 9:e103631. doi: 10.15252/embj.2019103631. PMID:32643828[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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