6e5n

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m (Protected "6e5n" [edit=sysop:move=sysop])
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'''Unreleased structure'''
 
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The entry 6e5n is ON HOLD until Paper Publication
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==Solution structure of human Myosin VI isoform 3 (1050-1131) in complex with Clathrin light chain a (46-61)==
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<StructureSection load='6e5n' size='340' side='right'caption='[[6e5n]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
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Authors:
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== Structural highlights ==
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<table><tr><td colspan='2'>[[6e5n]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6E5N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6E5N FirstGlance]. <br>
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Description:
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</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6e5n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6e5n OCA], [http://pdbe.org/6e5n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6e5n RCSB], [http://www.ebi.ac.uk/pdbsum/6e5n PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6e5n ProSAT]</span></td></tr>
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[[Category: Unreleased Structures]]
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</table>
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== Disease ==
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[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Autosomal dominant non-syndromic sensorineural deafness type DFNA;Autosomal recessive non-syndromic sensorineural deafness type DFNB;Progressive sensorineural hearing loss - hypertrophic cardiomyopathy. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry. The disease is caused by mutations affecting the gene represented in this entry.
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== Function ==
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[[http://www.uniprot.org/uniprot/MYO6_HUMAN MYO6_HUMAN]] Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Myosin 6 is a reverse-direction motor protein that moves towards the minus-end of actin filaments. Has slow rate of actin-activated ADP release due to weak ATP binding. Functions in a variety of intracellular processes such as vesicular membrane trafficking and cell migration. Required for the structural integrity of the Golgi apparatus via the p53-dependent pro-survival pathway. Appears to be involved in a very early step of clathrin-mediated endocytosis in polarized epithelial cells. May act as a regulator of F-actin dynamics. May play a role in transporting DAB2 from the plasma membrane to specific cellular targets. Required for structural integrity of inner ear hair cells (By similarity).<ref>PMID:10519557</ref> <ref>PMID:11447109</ref> <ref>PMID:16507995</ref> <ref>PMID:16949370</ref> [[http://www.uniprot.org/uniprot/CLCA_HUMAN CLCA_HUMAN]] Clathrin is the major protein of the polyhedral coat of coated pits and vesicles. Acts as component of the TACC3/ch-TOG/clathrin complex proposed to contribute to stabilization of kinetochore fibers of the mitotic spindle by acting as inter-microtubule bridge (PubMed:15858577, PubMed:21297582).<ref>PMID:15858577</ref> <ref>PMID:21297582</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: Large Structures]]
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[[Category: Buel, G R]]
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[[Category: Walters, K J]]
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[[Category: Clathrin]]
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[[Category: Endocytosis]]
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[[Category: Motor protein]]
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[[Category: Myosin]]
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[[Category: Trafficking]]

Revision as of 15:15, 20 November 2019

Solution structure of human Myosin VI isoform 3 (1050-1131) in complex with Clathrin light chain a (46-61)

PDB ID 6e5n

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