Junker, Andreas

[["dc.bibliographiccitation.firstpage","3738"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","FEBS Letters"],["dc.bibliographiccitation.lastpage","3746"],["dc.bibliographiccitation.volume","585"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T08:49:09Z"],["dc.date.available","2018-11-07T08:49:09Z"],["dc.date.issued","2011"],["dc.description.abstract","MicroRNAs (miRNAs) comprise a group of several hundred, small non-coding RNA molecules with a fundamental influence on the regulation of gene expression. Certain miRNAs are altered in blood cells of multiple sclerosis (MS), and active and inactive MS brain lesions have distinct miRNA expression profiles. Several miRNAs such as miR-155 or miR-326 are considerably overexpressed in active MS lesions versus controls, and mice lacking these miRNAs either through knock-out (miR-155) or by in vivo silencing (miR-326) show a reduction of symptoms in experimental autoimmune encephalomyelitis (EAE), a model system for multiple sclerosis. This review describes miRNAs regulated in the blood or in brain lesions of MS patients in the context of their previously described functions in physiology and pathophysiology. (C) 2011 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies."],["dc.identifier.doi","10.1016/j.febslet.2011.03.052"],["dc.identifier.isi","000297318000019"],["dc.identifier.pmid","21453702"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21390"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-3468"],["dc.relation.issn","0014-5793"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Pathophysiology of translational regulation by microRNAs in multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T09:33:35Z"],["dc.date.available","2018-11-07T09:33:35Z"],["dc.date.issued","2014"],["dc.format.extent","129"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.346"],["dc.identifier.isi","000345192100336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31999"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Axonal damage and protection during early remyelination in multiple sclerosis and an animal model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","796"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Macromolecular Rapid Communications"],["dc.bibliographiccitation.lastpage","802"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Buback, M."],["dc.contributor.author","Junkers, T."],["dc.contributor.author","Vana, P."],["dc.date.accessioned","2018-11-07T11:00:23Z"],["dc.date.available","2018-11-07T11:00:23Z"],["dc.date.issued","2005"],["dc.description.abstract","A novel method combining RAFT polymerization with pulsed-laser initiation for determining chain-length dependent termination rate coefficients, k(t), is presented. Degenerative chain-transfer in RAFT enables single-pulse pulsed-laser polymerization (SP-PLP) traces to be measured on systems with a narrow radical distribution that remains essentially unchanged during the experiment. SP-PLP-RAFT experiments at different polymerization times allow for determining kt as a function of chain length via classical kinetics assuming chain-length independent k(t)."],["dc.identifier.doi","10.1002/marc.200500067"],["dc.identifier.isi","000229424200005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50904"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-v C H Verlag Gmbh"],["dc.relation.issn","1022-1336"],["dc.title","Laser single pulse initiated RAFT polymerization for assessing chain-length dependent radical termination kinetics"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Mohan, Hema"],["dc.contributor.author","Friese, Anita"],["dc.contributor.author","Albrecht, Stefanie"],["dc.contributor.author","Krumbholz, Markus"],["dc.contributor.author","Elliott, Christina L"],["dc.contributor.author","Arthur, Ariel"],["dc.contributor.author","Menon, Ramesh"],["dc.contributor.author","Farina, Cinthia"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Meinl, Edgar"],["dc.date.accessioned","2021-06-01T10:48:07Z"],["dc.date.available","2021-06-01T10:48:07Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1186/s40478-014-0168-9"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85831"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2051-5960"],["dc.title","Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","56"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Reviews Neurology"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Hohlfeld, Reinhard"],["dc.contributor.author","Meinl, Edgar"],["dc.date.accessioned","2018-11-07T09:01:45Z"],["dc.date.available","2018-11-07T09:01:45Z"],["dc.date.issued","2011"],["dc.description.abstract","Several hundred microRNAs (miRNAs) fine-tune the expression of approximately half of all human genes. Recent studies have revealed that miRNA profiles in blood cells become altered in multiple sclerosis (MS), and that active and inactive MS lesions have distinct miRNA expression patterns. The dysregulated miRNAs in MS lesions seem to be associated with astrocytes and infiltrating immune cells, and might unleash local macrophages through downregulation of the self-recognition signal CD47. The expression of miRNA-326 in blood cells has been reported to increase during relapses. This miRNA promotes T helper 17 cell differentiation and is highly abundant in active MS lesions. miRNAs are needed for maintenance of the myelin sheath, and the absence of such molecules results in axonal damage in mice. miRNA-219 and other miRNAs promote oligodendrocyte differentiation. Here, we discuss the possible contribution of miRNAs to MS pathogenesis. An improved understanding of this contribution should help to identify novel therapeutic targets and biomarkers for this disease."],["dc.identifier.doi","10.1038/nrneurol.2010.179"],["dc.identifier.isi","000286099300012"],["dc.identifier.pmid","21151203"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24509"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1759-4758"],["dc.title","The emerging role of microRNAs in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","246"],["dc.contributor.author","Lescher, Juliane"],["dc.contributor.author","Paap, Franziska"],["dc.contributor.author","Schultz, Verena"],["dc.contributor.author","Redenbach, Laura"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Here we demonstrate that miRNA regulation in marmoset (Callithrix jacchus) and C57/BL6 mouse EAE lesions largely resembles miRNA regulation in active human MS lesions. Detailed quantitative PCR analyses of the most up- and downregulated miRNAs of active human MS lesions in dissected lesions from marmoset EAE brains and inflamed spinal cords of EAE mice revealed that the conserved and highly regulated miRNAs, miRNA-155, miRNA-142-3p, miRNA-146a, miRNA-146b and miRNA-21, turned out to be similarly upregulated in marmoset and mouse EAE lesions. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2012.02.012"],["dc.identifier.gro","3142535"],["dc.identifier.isi","000304026900004"],["dc.identifier.pmid","22445295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8897"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","MicroRNA regulation in experimental autoimmune encephalomyelitis in mice and marmosets resembles regulation in human multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","760"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","18"],["dc.contributor.affiliation","Voigt, David; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, david-voigt@gmx.net"],["dc.contributor.affiliation","Scheidt, Uta; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, uscheidt@med.uni-goettingen.de"],["dc.contributor.affiliation","Derfuss, Tobias; \t\t \r\n\t\t Neurologic Clinic and Policlinic, University Hospital Basel, Basel 4031, Switzerland, tobias.derfuss@usb.ch"],["dc.contributor.affiliation","Brück, Wolfgang; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center, Robert-Koch-Straße 40, Göttingen 37075, Germany, wbrueck@med.uni-goettingen.de"],["dc.contributor.affiliation","Junker, Andreas; \t\t \r\n\t\t Institute of Neuropathology, University Hospital Essen, Hufelandstr. 55, Essen 45122, Germany, andreas.junker@uk-essen.de"],["dc.contributor.author","Voigt, David"],["dc.contributor.author","Scheidt, Uta"],["dc.contributor.author","Derfuss, Tobias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Junker, Andreas"],["dc.date.accessioned","2018-11-07T10:25:12Z"],["dc.date.available","2018-11-07T10:25:12Z"],["dc.date.issued","2017"],["dc.date.updated","2022-09-05T16:09:31Z"],["dc.description.abstract","Multiple sclerosis is a chronic inflammatory disease of the central nervous system, characterized by demyelination and axonal damage as well as neuronal degeneration. Since oxygen-derived free radicals are an important factor leading to tissue damage in inflammatory multiple sclerosis (MS) lesions, research on antioxidative systems is essential to identify endogenous factors which can possibly counteract oxidative damage. As an important scavenging enzyme family, peroxiredoxins (PRDXs) play a crucial role in preventing oxidative damage; however little is known about their expression and function in MS lesions. In the present study we examined the expression of PRDX2 in white matter lesions of MS patients with long-standing, chronic disease. PRDX2 expression was investigated by immunohistochemistry in the context of oxidative stress and inflammation (determined by microglia/macrophage and T cell infiltration) in ten MS autopsy cases as well as seven control autopsy cases. PRDX2 was found to be upregulated in white matter MS lesions mainly in astrocytes, and its expression level was positively correlated with the degree of inflammation and oxidative stress. Our data suggest that PRDX2 expression contributes to the resistance of astrocytes against oxidative damage."],["dc.identifier.doi","10.3390/ijms18040760"],["dc.identifier.isi","000402639400085"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42804"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Mdpi Ag"],["dc.relation.eissn","1422-0067"],["dc.relation.issn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Expression of the Antioxidative Enzyme Peroxiredoxin 2 in Multiple Sclerosis Lesions in Relation to Inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","523"],["dc.bibliographiccitation.lastpage","537"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.editor","Lawrie, Charles H."],["dc.date.accessioned","2021-12-08T12:28:28Z"],["dc.date.available","2021-12-08T12:28:28Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1002/9781118300312.ch32"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95710"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.publisher","John Wiley & Sons, Inc."],["dc.publisher.place","Hoboken, NJ, USA"],["dc.relation.eisbn","9781118300312"],["dc.relation.isbn","9781118300398"],["dc.relation.ispartof","MicroRNAs in Medicine"],["dc.title","MicroRNA Regulation in Multiple Sclerosis"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","294"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","300"],["dc.bibliographiccitation.volume","80"],["dc.contributor.author","Gerdes, Lisa Ann"],["dc.contributor.author","Held, Kathrin"],["dc.contributor.author","Beltran, Eduardo"],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Prinz, Joerg C."],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","Tietze, Julia K."],["dc.contributor.author","Ertl-Wagner, Birgit"],["dc.contributor.author","Straube, Andreas"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Dornmair, Klaus"],["dc.contributor.author","Hohlfeld, Reinhard"],["dc.date.accessioned","2018-11-07T10:10:53Z"],["dc.date.available","2018-11-07T10:10:53Z"],["dc.date.issued","2016"],["dc.description.abstract","We investigated a patient who developed multiple sclerosis (MS) during treatment with the CTLA4-blocking antibody ipilimumab for metastatic melanoma. Initially he showed subclinical magnetic resonance imaging (MRI) changes (radiologically isolated syndrome). Two courses of ipilimumab were each followed by a clinical episode of MS, 1 of which was accompanied by a massive increase of MRI activity. Brain biopsy confirmed active, T-cell type MS. Quantitative next generation sequencing of T-cell receptor genes revealed distinct oligoclonal CD4(+) and CD8(+) T-cell repertoires in the primary melanoma and cerebrospinal fluid. Our results pinpoint the coinhibitory molecule CTLA4 as an immunological checkpoint and therapeutic target in MS."],["dc.identifier.doi","10.1002/ana.24715"],["dc.identifier.isi","000382402600013"],["dc.identifier.pmid","27351142"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14028"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39943"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","CTLA4 as Immunological Checkpoint in the Development of Multiple Sclerosis"],["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.firstpage","9497"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Macromolecules"],["dc.bibliographiccitation.lastpage","9508"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Junkers, T."],["dc.contributor.author","Theis, A."],["dc.contributor.author","Buback, M."],["dc.contributor.author","Davis, T. P."],["dc.contributor.author","Stenzel, M. H."],["dc.contributor.author","Vana, P."],["dc.contributor.author","Barner-Kowollik, C."],["dc.date.accessioned","2018-11-07T10:54:20Z"],["dc.date.available","2018-11-07T10:54:20Z"],["dc.date.issued","2005"],["dc.description.abstract","The chain-length dependence of the termination rate coefficient, k(t), in butyl acrylate free-radical polymerization has been determined by two independent methods, RAFT-SP-PLP and RAFT-CLD-T, both employing control of radical chain length by reversible addition fragmentation chain transfer (RAFT) polymerization. Within RAFT-SP-PLP, the polymerization induced by a laser single pulse is monitored via near-IR spectroscopy with a time resolution of microseconds. In RAFT-CLD-T, isothermal reaction rate measurements are carried out via DSC under stationary polymerization conditions. The resulting k(t) data refer to the situation of living/controlled radical polymerization, where both radical chain length and monomer conversion increase during the course of the reaction. The RAFT-SP-PLP measurements were carried out at 60 degrees C and two pressures, 5 and 1000 bar. The RAFT-CLD-T experiments were run at ambient pressure and at two temperatures, 60 and 80 degrees C, respectively. In absolute value, the termination rate coefficients for identical pressure and temperature deduced from the two methods differ by less than a factor of 2. For the dependence of k(t) on chain length, i, almost identical information is provided by the two techniques. The chain-length dependence of kt may be described by the power-law expression k(t)(i) = k(t)(1,1)i(-alpha) with, however, a being different for short-chain and long-chain radicals. RAFT-SP-PLP yields alpha(1) = 1.25 for the short-chain regime from 1 < i < 30, and alpha(2) = 0.22 for chain lengths above i = 50. RAFT-CLD-T results in alpha(1) = 1.04 and alpha(2) = 0.20 in identical chain length regimes. kt(1,1) values are found to be close to 1 x 10(9) L mol(-1) s(-1)."],["dc.identifier.doi","10.1021/ma051485k"],["dc.identifier.isi","000233225600015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49541"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Chemical Soc"],["dc.relation.issn","0024-9297"],["dc.title","Chain length dependent termination in butyl acrylate free-radical polymerization studied via stationary and pulsed laser initiated RAFT polymerization"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]