Motzkus, Dirk

[["dc.bibliographiccitation.artnumber","e75063"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Brameier, Markus"],["dc.contributor.author","Ibing, Wiebke"],["dc.contributor.author","Höfer, Katharina"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2019-07-09T11:54:33Z"],["dc.date.available","2019-07-09T11:54:33Z"],["dc.date.issued","2013-09-23"],["dc.description.abstract","Recent evidence indicates that regulatory small non-coding RNAs are not only components of eukaryotic cells and vesicles, but also reside within a number of different viruses including retroviral particles. Using ultra-deep sequencing we have comprehensively analyzed the content of simian immunodeficiency virions (SIV), which were compared to mock-control preparations. Our analysis revealed that more than 428,000 sequence reads matched the SIV mac239 genome sequence. Among these we could identify 12 virus-derived small RNAs (vsRNAs) that were highly abundant. Beside known retrovirus-enriched small RNAs, like 7SL-RNA, tRNALys3 and tRNALys isoacceptors, we also identified defined fragments derived from small ILF3/NF90-associated RNA snaR-A14, that were enriched more than 50 fold in SIV. We also found evidence that small nucleolar RNAs U2 and U12 were underrepresented in the SIV preparation, indicating that the relative number or the content of co-isolated exosomes was changed upon infection. Our comprehensive atlas of SIV-incorporated small RNAs provides a refined picture of the composition of retrovirions, which gives novel insights into viral packaging."],["dc.format.extent","16"],["dc.identifier.doi","10.1371/journal.pone.0075063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60676"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Mapping the Small RNA Content of Simian Immunodeficiency Virions (SIV)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","486"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Genomics"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Brameier, Markus"],["dc.contributor.author","Schmädicke, Ann-Christin"],["dc.contributor.author","Gilch, Sabine"],["dc.contributor.author","Schätzl, Hermann M."],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2019-07-09T11:53:50Z"],["dc.date.available","2019-07-09T11:53:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Prion diseases are neurodegenerative diseases that are characterized by the conversion of the cellular prion protein (PrPc) into a pathogenic isoform (PrPSc). It is known that neurodegeneration is often accompanied by the disturbance of cholesterol homeostasis. We have recently identified a set of genes that were upregulated after prion infection of N2a neuronal cells (Bach et al., 2009). Results We have now used ultra-deep sequencing technology to profile all microRNAs (miRNA) that could be associated with this effect in these N2a cells. Using stringent filters and normalization strategies we identified a small set of miRNAs that were up- or downregulated upon prion infection. Using bioinformatic tools we predicted whether the downregulated miRNAs could target mRNAs that have been previously identified to enhance cholesterol synthesis in these cells. Application of this joint profiling approach revealed that nine miRNAs potentially target cholesterol-related genes. Four of those miRNAs are localized in a miRNA-dense cluster on the mouse X-chromosome. Among these, twofold downregulation of mmu-miR-351 and mmu-miR-542-5p was confirmed by qRT-PCR. The same miRNAs were predicted as putative regulators of the sterol regulatory element-binding factor 2 (Srebf2), the low-density lipoprotein receptor (Ldlr) or the IPP isomerase. Conclusions The results demonstrate that joined profiling by ultra-deep sequencing is highly valuable to identify candidate miRNAs involved in prion-induced dysregulation of cholesterol homeostasis."],["dc.identifier.doi","10.1186/1471-2164-13-486"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8111"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60508"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","A genome-wide survey for prion-regulated miRNAs associated with cholesterol homeostasis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e86857"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Hotop, Sven-Kevin"],["dc.contributor.author","Abd El Wahed, Ahmed"],["dc.contributor.author","Beutling, Ulrike"],["dc.contributor.author","Jentsch, Dieter"],["dc.contributor.author","Motzkus, Dirk"],["dc.contributor.author","Frank, Ronald"],["dc.contributor.author","Hunsmann, Gerhard"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Fritz, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:44:53Z"],["dc.date.available","2018-11-07T09:44:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Herpes B virus (or Herpesvirus simiae or Macacine herpesvirus 1) is endemic in many populations of macaques, both in the wild and in captivity. The virus elicits only mild clinical symptoms (if any) in monkeys, but can be transmitted by various routes, most commonly via bites, to humans where it causes viral encephalitis with a high mortality rate. Hence, herpes B constitutes a considerable occupational hazard for animal caretakers, veterinarians and laboratory personnel. Efforts are therefore being made to reduce the risk of zoonotic infection and to improve prognosis after accidental exposure. Among the measures envisaged are serological surveillance of monkey colonies and specific diagnosis of herpes B zoonosis against a background of antibodies recognizing the closely related human herpes simplex virus (HSV). 422 pentadecapeptides covering, in an overlapping fashion, the entire amino acid sequences of herpes B proteins gB and gD were synthesized and immobilized on glass slides. Antibodies present in monkey sera that bind to subsets of the peptide collection were detected by microserological techniques. With 42 different rhesus macaque sera, 114 individual responses to 18 different antibody target regions (ATRs) were recorded, 17 of which had not been described earlier. This finding may pave the way for a peptide-based, herpes B specific serological diagnostic test."],["dc.description.sponsorship","EUPRIM-Net under the EU [262443]"],["dc.identifier.doi","10.1371/journal.pone.0086857"],["dc.identifier.isi","000330621900043"],["dc.identifier.pmid","24497986"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9897"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34494"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Multiple Antibody Targets on Herpes B Glycoproteins B and D Identified by Screening Sera of Infected Rhesus Macaques with Peptide Microarrays"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","36"],["dc.bibliographiccitation.journal","Molecular Neurodegeneration"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Montag, Judith"],["dc.contributor.author","Hitt, Reiner"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Hunsmann, Gerhard"],["dc.contributor.author","Motzkus, Dirk"],["dc.date.accessioned","2018-11-07T11:25:35Z"],["dc.date.available","2018-11-07T11:25:35Z"],["dc.date.issued","2009"],["dc.description.abstract","The aim of our study was to analyze the differential expression of miRNAs in the brains of BSE-infected cynomolgus macaques as a model for Creutzfeldt-Jakob disease (CJD). MicroRNAs (miRNAs) are small noncoding RNAs regulating gene expression by mRNA targeting. Among other functions they contribute to neuronal development and survival. Recently, the lack of miRNA processing has been shown to promote neurodegeneration and deregulation of several miRNAs has been reported to be associated with Scrapie in mice. Therefore, we hypothesized that miRNAs are also regulated in response to human prion disease. We have applied miRNA-microarrays to identify deregulated miRNA candidates in brains of BSE-infected macaques. Shock-frozen brain sections of six BSE-infected and five non-infected macaques were used to validate regulated miRNA candidates by two independent qRT-PCR-based methods. Our study revealed significant upregulation of hsa-miR-342-3p and hsa-miR-494 in the brains of BSE-infected macaques compared to non-infected animals. In a pilot study we could show that hsa-miR-342-3p was also upregulated in brain samples of human type 1 and type 2 sporadic CJD. With respect to the reported regulation of this miRNA in Scrapie-infected mice, we propose that upregulation of hsa-miR-342-3p may be a general phenomenon in late stage prion disease and might be used as a novel marker for animal and human TSEs."],["dc.identifier.doi","10.1186/1750-1326-4-36"],["dc.identifier.isi","000269952200001"],["dc.identifier.pmid","19712440"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5783"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56654"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1750-1326"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Upregulation of miRNA hsa-miR-342-3p in experimental and idiopathic prion disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]