View source for 8xo6


==Crystal structure of measles virus fusion inhibitor MEK35GE complexed with F protein HR1 (HR1-42) (P21212 space group)==
<StructureSection load='8xo6' size='340' side='right'caption='[[8xo6]], [[Resolution|resolution]] 1.46&Aring;' scene=''>
== Structural highlights ==
<table><tr><td colspan='2'>[[8xo6]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Measles_virus_strain_Edmonston Measles virus strain Edmonston]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8XO6 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8XO6 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]] 1.457&#8491;</td></tr>
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ACE:ACETYL+GROUP'>ACE</scene>, <scene name='pdbligand=ACT:ACETATE+ION'>ACT</scene>, <scene name='pdbligand=NH2:AMINO+GROUP'>NH2</scene>, <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=8xo6 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8xo6 OCA], [https://pdbe.org/8xo6 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8xo6 RCSB], [https://www.ebi.ac.uk/pdbsum/8xo6 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8xo6 ProSAT]</span></td></tr>
</table>
== Function ==
[https://www.uniprot.org/uniprot/FUS_MEASE FUS_MEASE] Class I viral fusion protein. Under the current model, the protein has at least 3 conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state. During viral and plasma cell membrane fusion, the heptad repeat (HR) regions assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain. The formation of this structure appears to drive apposition and subsequent fusion of viral and plasma cell membranes. Directs fusion of viral and cellular membranes leading to delivery of the nucleocapsid into the cytoplasm. This fusion is pH independent and occurs directly at the outer cell membrane. During viral entry or virus-mediated fusion between infected cells and neighboring susceptible cells, the head domain of the H protein initially binds to its receptor and then the stalk region of the H protein transmits the fusion-triggering signal to the F protein (By similarity). Upon HN binding to its cellular receptor, the hydrophobic fusion peptide is unmasked and interacts with the cellular membrane, inducing the fusion between cell and virion membranes. Later in infection, F proteins expressed at the plasma membrane of infected cells could mediate fusion with adjacent cells to form syncytia, a cytopathic effect that could lead to tissue necrosis (By similarity).[UniProtKB:Q786F3]  Some hyperfusogenic isolates can induce membrane fusion in SLAM- and nectin-4-negative cells and are linked to fatal subacute sclerosing panencephalitis (SSPE) or measles inclusion body encephalitis (MIBE). The neuropathogenicity is closely associated with enhanced propagation mediated by cell-to-cell fusion in the brain, which is principally regulated by hyperfusogenic mutations of the viral F protein. Cell-to-cell transmission of the virus also occurs with hyperfusogenic isolates.[UniProtKB:Q786F3]
__TOC__
</StructureSection>
[[Category: Large Structures]]
[[Category: Measles virus strain Edmonston]]
[[Category: Nakatsu T]]
[[Category: Oishi S]]
[[Category: Takahara A]]