Now showing 1 - 2 of 2
  • 2013-02-28Journal Article
    [["dc.bibliographiccitation.artnumber","e57530"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Vadhvani, Mayur"],["dc.contributor.author","Schwedhelm-Domeyer, Nicola"],["dc.contributor.author","Mukherjee, Chaitali"],["dc.contributor.author","Stegmüller, Judith"],["dc.date.accessioned","2019-07-09T11:54:16Z"],["dc.date.available","2019-07-09T11:54:16Z"],["dc.date.issued","2013-02-28"],["dc.description.abstract","Neuronal development requires proper migration, polarization and establishment of axons and dendrites. Growing evidence identifies the ubiquitin proteasome system (UPS) with its numerous components as an important regulator of various aspects of neuronal development. F-box proteins are interchangeable subunits of the Cullin-1 based E3 ubiquitin ligase, but only a few family members have been studied. Here, we report that the centrosomal E3 ligase FBXO31-SCF (Skp1/ Cullin-1/F-box protein) regulates neuronal morphogenesis and axonal identity. In addition, we identified the polarity protein Par6c as a novel interaction partner and substrate targeted for proteasomal degradation in the control of axon but not dendrite growth. Finally, we ascribe a role for FBXO31 in dendrite growth and neuronal migration in the developing cerebellar cortex. Taken together, we uncovered the centrosomal E3 ligase FBXO31-SCF as a novel regulator of neuronal development."],["dc.format.extent","13"],["dc.identifier.doi","10.1371/journal.pone.0057530"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8725"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60609"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The Centrosomal E3 Ubiquitin Ligase FBXO31-SCF Regulates Neuronal Morphogenesis and Migration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2015Journal Article
    [["dc.bibliographiccitation.firstpage","1233"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","1236"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Heinrich, Ralf"],["dc.contributor.author","Monnheimer, Mathieu"],["dc.contributor.author","Gerhart, Simone"],["dc.contributor.author","Stegmüller, Judith"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:28Z"],["dc.date.available","2017-09-07T11:46:28Z"],["dc.date.issued","2015"],["dc.description.abstract","Traumatic brain injury causes progressive brain atrophy and cognitive decline. Surprisingly, an early treatment with erythropoietin (EPO) prevents these consequences of secondary neurodegeneration, but the mechanisms have remained obscure. Here we show by advanced imaging and innovative analytical tools that recombinant human EPO, a clinically established and neuroprotective growth factor, dampens microglial activity, as visualized also in vivo by a strongly attenuated injury-induced cellular motility."],["dc.identifier.doi","10.1038/jcbfm.2015.100"],["dc.identifier.gro","3150519"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7292"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject","ATP; brain injury; migration; process protrusion; Rac1"],["dc.title","Erythropoietin dampens injury-induced microglial motility"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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