Weishaupt, Jochen Hans

[["dc.bibliographiccitation.firstpage","1232"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pharmaceuticals"],["dc.bibliographiccitation.lastpage","1240"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.date.accessioned","2019-07-09T11:53:05Z"],["dc.date.available","2019-07-09T11:53:05Z"],["dc.date.issued","2010"],["dc.description.abstract","Cdk5 is essential for neuronal differentiation processes in the brain. Activation of Cdk5 requires the association with the mostly neuron-specific p35 or p39. Overactivation of CDK5 by cleavage of p35 into p25 is thought to be involved in neurodegenerative processes. Here, we have tested an approach to inhibit pathological Cdk5 activation with a Tat-linked dominant-negative fragment of p25. It reduced cell death induced by staurosporine and showed a tendency to alleviate manganese-induced cell death, while it did not protect against 6-OHDA toxicity. Our results suggest that the Tat technique is a suitable tool to inhibit dysregulated CDK5."],["dc.identifier.doi","10.3390/ph3041232"],["dc.identifier.fs","577416"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60337"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1424-8247"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Cell-Penetrating Fragments of the Cdk5 Regulatory Subunit Are Protective in Models of Neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.contributor.author","Weishaupt, Jochen Hans"],["dc.contributor.author","Dietz, Gunnar"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Frank, Tobias"],["dc.contributor.author","Schlachetzki, Johannes C. M."],["dc.contributor.author","Meuer, Katrin"],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Schneider, Armin"],["dc.date.accessioned","2019-07-10T08:13:27Z"],["dc.date.available","2019-07-10T08:13:27Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) plays a crucial role in controlling the number of neutrophil progenitor cells. Its function is mediated via the G-CSF receptor, which was recently found to be expressed also in the central nervous system. In addition, G-CSF provided neuroprotection in models of neuronal cell death. Here we used the retinal ganglion cell (RGC) axotomy model to compare effects of local and systemic application of neuroprotective molecules. Results: We found that the G-CSF receptor is robustly expressed by RGCs in vivo and in vitro. We thus evaluated G-CSF as a neuroprotectant for RGCs and found a dose-dependent neuroprotective effect of G-CSF on axotomized RGCs when given subcutaneously. As stem stell mobilization had previously been discussed as a possible contributor to the neuroprotective effects of G-CSF, we compared the local treatment of RGCs by injection of G-CSF into the vitreous body with systemic delivery by subcutaneous application. Both routes of application reduced retinal ganglion cell death to a comparable extent. Moreover, G-CSF enhanced the survival of immunopurified RGCs in vitro. Conclusion: We thus show that G-CSF neuroprotection is at least partially independent of potential systemic effects and provide further evidence that the clinically applicable G-CSF could become a treatment option for both neurodegenerative diseases and glaucoma"],["dc.identifier.fs","568091"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2202"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Both systemic and local application of granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]