Motzkus, Dirk

[["dc.bibliographiccitation.firstpage","1125"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","EMERGING INFECTIOUS DISEASES"],["dc.bibliographiccitation.lastpage","1127"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Schrod, Annette"],["dc.contributor.author","Hunsmann, Gerhard"],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2018-11-07T09:22:36Z"],["dc.date.available","2018-11-07T09:22:36Z"],["dc.date.issued","2013"],["dc.description.abstract","To estimate the effect of the variability of prion disease onset on primary bovine spongiform encephalopathy transmission to humans, we studied 6 cynomolgus macaques. The preclinical incubation period was significantly prolonged in 2 animals, implying that onset of variant Creutzfeldt-Jacob disease in humans could be more diverse than previously expected."],["dc.description.sponsorship","European Union [QLK1-CT-2002-01096, BMH4-CT-98-6029]"],["dc.identifier.doi","10.3201/eid1907.120438"],["dc.identifier.isi","000328173600017"],["dc.identifier.pmid","23764183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29388"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Centers Disease Control"],["dc.relation.issn","1080-6059"],["dc.relation.issn","1080-6040"],["dc.title","Asynchronous Onset of Clinical Disease in BSE-Infected Macaques"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Vanni, Silvia"],["dc.contributor.author","Barbisin, Maura"],["dc.contributor.author","Schmaedicke, Ann-Christin"],["dc.contributor.author","Motzkus, Dirk"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Legname, Giuseppe"],["dc.date.accessioned","2018-11-07T09:41:29Z"],["dc.date.available","2018-11-07T09:41:29Z"],["dc.date.issued","2014"],["dc.format.extent","93"],["dc.identifier.isi","000340614900202"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33744"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","Gene expression profiling of brains from bovine spongiform encephalopathy (BSE)-infected cynomolgus macaques"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurodegeneration"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Greenwood, Alex D"],["dc.contributor.author","Vincendeau, Michelle"],["dc.contributor.author","Schmädicke, Ann-Christin"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Seifarth, Wolfgang"],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2022-10-06T13:26:12Z"],["dc.date.available","2022-10-06T13:26:12Z"],["dc.date.issued","2011"],["dc.description.abstract","Abstract\n \n Background\n Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease.\n \n \n Results\n \n Cynomolgus macaques (\n Macaca fasicularis\n ) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the\n basis pontis\n and\n vermis cerebelli\n of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques.\n \n \n \n Conclusions\n We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration."],["dc.identifier.doi","10.1186/1750-1326-6-44"],["dc.identifier.pii","204"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115024"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1750-1326"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Bovine spongiform encephalopathy infection alters endogenous retrovirus expression in distinct brain regions of cynomolgus macaques (Macaca fascicularis)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","434"],["dc.bibliographiccitation.journal","BMC Genomics"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Barbisin, Maura"],["dc.contributor.author","Vanni, Silvia"],["dc.contributor.author","Schmaedicke, Ann-Christin"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Motzkus, Dirk"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Legname, Giuseppe"],["dc.date.accessioned","2018-11-07T09:38:59Z"],["dc.date.available","2018-11-07T09:38:59Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Prion diseases are fatal neurodegenerative disorders whose pathogenesis mechanisms are not fully understood. In this context, the analysis of gene expression alterations occurring in prion-infected animals represents a powerful tool that may contribute to unravel the molecular basis of prion diseases and therefore discover novel potential targets for diagnosis and therapeutics. Here we present the first large-scale transcriptional profiling of brains from BSE-infected cynomolgus macaques, which are an excellent model for human prion disorders. Results: The study was conducted using the GeneChip (R) Rhesus Macaque Genome Array and revealed 300 transcripts with expression changes greater than twofold. Among these, the bioinformatics analysis identified 86 genes with known functions, most of which are involved in cellular development, cell death and survival, lipid homeostasis, and acute phase response signaling. RT-qPCR was performed on selected gene transcripts in order to validate the differential expression in infected animals versus controls. The results obtained with the microarray technology were confirmed and a gene signature was identified. In brief, HBB and HBA2 were down-regulated in infected macaques, whereas TTR, APOC1 and SERPINA3 were up-regulated. Conclusions: Some genes involved in oxygen or lipid transport and in innate immunity were found to be dysregulated in prion infected macaques. These genes are known to be involved in other neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. Our results may facilitate the identification of potential disease biomarkers for many neurodegenerative diseases."],["dc.identifier.doi","10.1186/1471-2164-15-434"],["dc.identifier.isi","000338257000001"],["dc.identifier.pmid","24898206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33181"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2164"],["dc.title","Gene expression profiling of brains from bovine spongiform encephalopathy (BSE)-infected cynomolgus macaques"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Cell Research"],["dc.bibliographiccitation.lastpage","79"],["dc.bibliographiccitation.volume","254"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Singh, Prim B."],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2018-11-07T10:58:25Z"],["dc.date.available","2018-11-07T10:58:25Z"],["dc.date.issued","2000"],["dc.description.abstract","In mature sperm the normal nucleosomal packaging of DNA found in somatic and meiotic cells is transformed into a highly condensed form of chromatin which consists mostly of nucleoprotamines. Although sperm DNA is highly condensed it is nevertheless packaged into a highly defined nuclear architecture which may be organized by the heterochromatic chromocenter, One major component of heterochromatin is the heterochromatin protein 1 which is involved in epigenetic gene silencing. In order to investigate the possible involvement of heterochromatin protein in higher order organization of sperm DNA we studied the localization of the muring homologue of heterochromatin protein 1, M31, during chromatin reorganization in male germ cell differentiation. Each cell type in the testis showed a unique distribution pattern of M31, Colocalization to the heterochromatic regions were found in Sertoli cells, in midstage pachytene spermatocytes, and in round spermatids in which M31 localizes to the centromeric chromocenter. M31 cannot be detected in elongated spermatids or mature spermatozoa immunocytologically, but could be detected in mature spermatozoa by Western blotting, We suggest that M31, a nuclear protein involved in the organization of chromatin architecture, is involved in higher order organization of sperm DNA (C) 2000 Academic Press."],["dc.identifier.doi","10.1006/excr.1999.4729"],["dc.identifier.isi","000085233500008"],["dc.identifier.pmid","10623467"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50475"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-4827"],["dc.title","The murine heterochromatin protein M31 is associated with the chromocenter in round spermatids and is a component of mature spermatozoa"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schiller, Barbara"],["dc.contributor.author","Schmaedicke, Ann-Christin"],["dc.contributor.author","Schuder, Angelina"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Dudas, Sandor"],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2018-11-07T09:41:29Z"],["dc.date.available","2018-11-07T09:41:29Z"],["dc.date.issued","2014"],["dc.format.extent","100"],["dc.identifier.isi","000340614900216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33745"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","Adaptation of RT-QuIC for the detection of BSE in cattle"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","77"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Retrovirology"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Mußil, Bianka"],["dc.contributor.author","Sauermann, Ulrike"],["dc.contributor.author","Motzkus, Dirk"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Sopper, Sieghart"],["dc.date.accessioned","2021-06-01T10:48:00Z"],["dc.date.available","2021-06-01T10:48:00Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1186/1742-4690-8-77"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85797"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","1742-4690"],["dc.title","Increased APOBEC3G and APOBEC3F expression is associated with low viral load and prolonged survival in simian immunodeficiency virus infected rhesus monkeys"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]