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dc.contributor.authorOrme, MHen_US
dc.contributor.authorLiccardi, Gen_US
dc.contributor.authorModerau, Nen_US
dc.contributor.authorFeltham, Ren_US
dc.contributor.authorWicky-John, Sen_US
dc.contributor.authorTenev, Ten_US
dc.contributor.authorAram, Len_US
dc.contributor.authorWilson, Ren_US
dc.contributor.authorBianchi, Ken_US
dc.contributor.authorMorris, Oen_US
dc.contributor.authorMonteiro Domingues, Cen_US
dc.contributor.authorRobertson, Den_US
dc.contributor.authorTare, Men_US
dc.contributor.authorWepf, Aen_US
dc.contributor.authorWilliams, Den_US
dc.contributor.authorBergmann, Aen_US
dc.contributor.authorGstaiger, Men_US
dc.contributor.authorArama, Een_US
dc.contributor.authorRibeiro, PSen_US
dc.contributor.authorMeier, Pen_US
dc.date.accessioned2016-09-05T11:32:22Z
dc.date.issued2016-03-10en_US
dc.identifier.citationNature communications, 2016, 7 pp. 10972 - ?en_US
dc.identifier.issn2041-1723en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/93
dc.identifier.eissn2041-1723en_US
dc.identifier.doi10.1038/ncomms10972en_US
dc.description.abstractCaspases provide vital links in non-apoptotic regulatory networks controlling inflammation, compensatory proliferation, morphology and cell migration. How caspases are activated under non-apoptotic conditions and process a selective set of substrates without killing the cell remain enigmatic. Here we find that the Drosophila unconventional myosin CRINKLED (CK) selectively interacts with the initiator caspase DRONC and regulates some of its non-apoptotic functions. Loss of CK in the arista, border cells or proneural clusters of the wing imaginal discs affects DRONC-dependent patterning. Our data indicate that CK acts as substrate adaptor, recruiting SHAGGY46/GSK3-β to DRONC, thereby facilitating caspase-mediated cleavage and localized modulation of kinase activity. Similarly, the mammalian CK counterpart, MYO7A, binds to and impinges on CASPASE-8, revealing a new regulatory axis affecting receptor interacting protein kinase-1 (RIPK1)>CASPASE-8 signalling. Together, our results expose a conserved role for unconventional myosins in transducing caspase-dependent regulation of kinases, allowing them to take part in specific signalling events.en_US
dc.formatElectronicen_US
dc.format.extent10972 - ?en_US
dc.languageengen_US
dc.language.isoengen_US
dc.subjectCell Line, Tumoren_US
dc.subjectNIH 3T3 Cellsen_US
dc.subjectAnimalsen_US
dc.subjectHumansen_US
dc.subjectMiceen_US
dc.subjectDrosophila melanogasteren_US
dc.subjectMyosinsen_US
dc.subjectCaspasesen_US
dc.subjectGlycogen Synthase Kinase 3en_US
dc.subjectDrosophila Proteinsen_US
dc.subjectMicroscopy, Confocalen_US
dc.subjectFlow Cytometryen_US
dc.subjectImmunoprecipitationen_US
dc.subjectSignal Transductionen_US
dc.subjectCaspase 8en_US
dc.subjectReceptor-Interacting Protein Serine-Threonine Kinasesen_US
dc.subjectWings, Animalen_US
dc.subjectGlycogen Synthase Kinase 3 betaen_US
dc.subjectMyosin VIIaen_US
dc.titleThe unconventional myosin CRINKLED and its mammalian orthologue MYO7A regulate caspases in their signalling roles.en_US
dc.typeJournal Article
dcterms.dateAccepted2016-02-05en_US
rioxxterms.versionofrecord10.1038/ncomms10972en_US
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0en_US
rioxxterms.licenseref.startdate2016-03-10en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfNature communicationsen_US
pubs.notesNo embargoen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Cell Death and Immunity
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Target Discovery & Apoptosis
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Target Discovery & Apoptosis
pubs.publication-statusPublisheden_US
pubs.volume7en_US
pubs.embargo.termsNo embargoen_US
icr.researchteamCell Death and Immunityen_US
icr.researchteamTarget Discovery & Apoptosisen_US
dc.contributor.icrauthorMeier, Pascalen_US
dc.contributor.icrauthorMorris, Ottoen_US


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