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Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-166
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dc.contributor.authorMikuličić, Snježana-
dc.contributor.authorFinke, Jérôme-
dc.contributor.authorBoukhallouk, Fatima-
dc.contributor.authorWüstenhagen, Elena-
dc.contributor.authorSons, Dominik-
dc.contributor.authorHomsi, Yahya-
dc.contributor.authorReiss, Karina-
dc.contributor.authorLang, Thorsten-
dc.contributor.authorFlorin, Luise-
dc.date.accessioned2019-07-08T11:12:53Z-
dc.date.available2019-07-08T13:12:53Z-
dc.date.issued2019-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/168-
dc.description.abstractOncogenic human papillomaviruses (HPV) are small DNA viruses that infect keratinocytes. After HPV binding to cell surface receptors, a cascade of molecular interactions mediates the infectious cellular internalization of virus particles. Aside from the virus itself, important molecular players involved in virus entry include the tetraspanin CD151 and the epidermal growth factor receptor (EGFR). To date, it is unknown how these components are coordinated in space and time. Here, we studied plasma membrane dynamics of CD151 and EGFR and the HPV16 capsid during the early phase of infection. We find that the proteinase ADAM17 activates the extracellular signal-regulated kinases (ERK1/2) pathway by the shedding of growth factors which triggers the formation of an endocytic entry platform. Infectious endocytic entry platforms carrying virus particles consist of two-fold larger CD151 domains containing the EGFR. Our finding clearly dissects initial virus binding from ADAM17-dependent assembly of a HPV/CD151/EGFR entry platform.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleADAM17-dependent signaling is required for oncogenic human papillomavirus entry platform assemblyen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-publ-591345-
dc.identifier.doihttp://doi.org/10.25358/openscience-166-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleeLife-
jgu.journal.volume8-
jgu.pages.alternativee44345-
jgu.publisher.year2019-
jgu.publisher.nameeLife Sciences Publications-
jgu.publisher.placeCambridge-
jgu.publisher.urihttp://dx.doi.org/10.7554/eLife.44345.001-
jgu.publisher.issn2050-084X-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2019-07-08T11:12:53Z-
opus.date.modified2019-07-09T08:35:31Z-
opus.date.available2019-07-08T13:12:53-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Institut für Virologiede_DE
opus.organisation.stringFB 04: Medizin: Forschungszentrum für Immuntherapie (FZI)de_DE
opus.organisation.stringFB 04: Medizin: Institut für Medizinische Mikrobiologie und Hygienede_DE
opus.identifier.opusid59134-
opus.institute.number0409-
opus.institute.number0476-
opus.institute.number0408-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedBoukhallouk, Fatima-
opus.affiliatedFlorin, Luise-
jgu.publisher.doi10.7554/eLife.44345.001
jgu.organisation.rorhttps://ror.org/023b0x485
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