Kramann, Nadine

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kramann, N."],["dc.contributor.author","Menken, Lena"],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Hanisch, U-K"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Wegner, C."],["dc.date.accessioned","2018-11-07T09:35:28Z"],["dc.date.available","2018-11-07T09:35:28Z"],["dc.date.issued","2014"],["dc.format.extent","382"],["dc.identifier.isi","000354441300878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32389"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","Joint ACTRIMS-ECTRIMS Meeting"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Laquinimod treatment prevents cuprizone-induced demyelination independent of Toll-like receptor signaling via MyD88 and TRIF"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0168174"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Huhndorf, Monika"],["dc.contributor.author","Moussavi, Amir"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Will, Olga Maria"],["dc.contributor.author","Hattermann, Kirsten"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Jansen, Olav"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.editor","Sherman, Jonathan H."],["dc.date.accessioned","2017-09-07T11:44:48Z"],["dc.date.available","2017-09-07T11:44:48Z"],["dc.date.issued","2017"],["dc.description.abstract","ObjectivesAngiogenesis and anti-angiogenetic medications play an important role in progression and therapy of glioblastoma. In this context, in vivo characterization of the blood-brain-barrier and tumor vascularization may be important for individual prognosis and therapy optimization.MethodsWe analyzed perfusion and capillary permeability of C6-gliomas in rats at different stages of tumor-growth by contrast enhanced MRI and dynamic susceptibility contrast (DSC) MRI at 7 Tesla. The analyses included maps of relative cerebral blood volume (CBV) and signal recovery derived from DSC data over a time period of up to 35 days after tumor cell injections.ResultsIn all rats tumor progression was accompanied by temporal and spatial changes in CBV and capillary permeability. A leakage of the blood-brain barrier (slow contrast enhancement) was observed as soon as the tumor became detectable on T2-weighted images. Interestingly, areas of strong capillary permeability (fast signal enhancement) were predominantly localized in the center of the tumor. In contrast, the tumor rim was dominated by an increased CBV and showed the highest vessel density compared to the tumor center and the contralateral hemisphere as confirmed by histology.ConclusionSubstantial regional differences in the tumor highlight the importance of parameter maps in contrast or in addition to region-of-interest analyses. The data vividly illustrate how MRI including contrast-enhanced and DSC-MRI may contribute to a better understanding of tumor development."],["dc.identifier.doi","10.1371/journal.pone.0168174"],["dc.identifier.gro","3150343"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7096"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Alterations of the Blood-Brain Barrier and Regional Perfusion in Tumor Development: MRI Insights from a Rat C6 Glioma Model"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","88"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","96"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2017-09-07T11:46:22Z"],["dc.date.available","2017-09-07T11:46:22Z"],["dc.date.issued","2014"],["dc.description.abstract","Aim Activation of the kinase RAF and its downstream targets leads to cardiomyocyte hypertrophy. It has been hypothesized that B-RAF might be the main activator of MEK in various cell types. Therefore, the aim of this study was to investigate the role of B-RAF and its modulating factors in cardiomyocyte hypertrophy. Methods and results Neonatal rat cardiomyocytes were pre-treated with and without the specific B-RAF inhibitor SB590885 and then stimulated with phenylephrine to induce hypertrophy. Inhibition of B-RAF completely impeded the hypertrophic response and led to a significant reduction of MEK1/2 phosphorylation. By applying a eukaryotic cDNA expression screen, based on a dual-luciferase reporter assay for B-RAF activity measurement, we identified RCN1 as a new negative modulator of B-RAF activity. Adenovirus-mediated overexpression of reticulocalbin 1 (RCN1) completely impeded phenylephrine-induced hypertrophy and led to significantly reduced MEK1/2 phosphorylation. Conversely, adenoviral knockdown of RCN1 with a specific synthetic miRNA induced cardiomyocyte hypertrophy and significantly increased MEK1/2 phosphorylation. Conclusions In summary, our results show that the inhibition of B-RAF abolishes cardiomyocyte hypertrophy and we identified RCN1 as novel negative modulator of cardiomyocyte hypertrophy by inhibition of the mitogen-activated protein kinase signalling cascade. Our results show that B-RAF kinase activity is essential for cardiac hypertrophy and RCN1, its newly identified negative regulator, abolishes hypertrophic response of cardiomyocytes in vitro."],["dc.identifier.doi","10.1093/cvr/cvu024"],["dc.identifier.gro","3142156"],["dc.identifier.isi","000334105600012"],["dc.identifier.pmid","24492844"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5155"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.title","B-RAF and its novel negative regulator reticulocalbin 1 (RCN1) modulates cardiomyocyte hypertrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","411"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","424"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Pham, Trinh"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Hayardeny, Liat"],["dc.contributor.author","Piryatinsky, Victor"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Brakelmann, Lars"],["dc.contributor.author","Hagemeier, Karin"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","John, Gareth R."],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:06:50Z"],["dc.date.available","2018-11-07T09:06:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Laquinimod (LAQ) is a new oral immunomodulatory compound that reduces relapse rate, brain atrophy and disability progression in multiple sclerosis (MS). LAQ has well-documented effects on inflammation in the periphery, but little is known about its direct activity within the central nervous system (CNS). To elucidate the impact of LAQ on CNS-intrinsic inflammation, we investigated the effects of LAQ on cuprizone-induced demyelination in mice in vivo and on primary CNS cells in vitro. Demyelination, inflammation, axonal damage and glial pathology were evaluated in LAQ-treated wild type and Rag-1-deficient mice after cuprizone challenge. Using primary cells we tested for effects of LAQ on oligodendroglial survival as well as on cytokine secretion and NF-kappa B activation in astrocytes and microglia. LAQ prevented cuprizone-induced demyelination, microglial activation, axonal transections, reactive gliosis and oligodendroglial apoptoses in wild type and Rag-1-deficient mice. LAQ significantly decreased pro-inflammatory factors in stimulated astrocytes, but not in microglia. Oligodendroglial survival was not affected by LAQ in vitro. Astrocytic, but not microglial, NF-kappa B activation was markedly reduced by LAQ as evidenced by NF-kappa B reporter assay. LAQ also significantly decreased astrocytic NF-kappa B activation in cuprizone-treated mice. Our data indicate that LAQ prevents cuprizone-induced demyelination by attenuating astrocytic NF-kappa B activation. These effects are CNS-intrinsic and not mediated by peripheral immune cells. Therefore, LAQ downregulation of the astrocytic pro-inflammatory response may be an important mechanism underlying its protective effects on myelin, oligodendrocytes and axons. Modulation of astrocyte activation may be an attractive therapeutic target to prevent tissue damage in MS."],["dc.identifier.doi","10.1007/s00401-012-1009-1"],["dc.identifier.isi","000307757200010"],["dc.identifier.pmid","22766690"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25641"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Reduced astrocytic NF-kappa B activation by laquinimod protects from cuprizone-induced demyelination"],["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","28"],["dc.bibliographiccitation.journal","BMC Cell Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Burnicka-Turek, Ozanna"],["dc.contributor.author","Kata, Aleksandra"],["dc.contributor.author","Buyandelger, Byambajav"],["dc.contributor.author","Ebermann, Linda"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T08:44:00Z"],["dc.date.available","2018-11-07T08:44:00Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Pelota (PELO) is an evolutionary conserved protein, which has been reported to be involved in the regulation of cell proliferation and stem cell self-renewal. Recent studies revealed the essential role of PELO in the No-Go mRNA decay, by which mRNA with translational stall are endonucleotically cleaved and degraded. Further, PELO-deficient mice die early during gastrulation due to defects in cell proliferation and/or differentiation. Results: We show here that PELO is associated with actin microfilaments of mammalian cells. Overexpression of human PELO in Hep2G cells had prominent effect on cell growth, cytoskeleton organization and cell spreading. To find proteins interacting with PELO, full-length human PELO cDNA was used as a bait in a yeast two-hybrid screening assay. Partial sequences of HAX1, EIF3G and SRPX protein were identified as PELO-interacting partners from the screening. The interactions between PELO and HAX1, EIF3G and SRPX were confirmed in vitro by GST pull-down assays and in vivo by co-immunoprecipitation. Furthermore, the PELO interaction domain was mapped to residues 268-385 containing the c-terminal and acidic tail domain. By bimolecular fluorescence complementation assay (BiFC), we found that protein complexes resulting from the interactions between PELO and either HAX1, EIF3G or SRPX were mainly localized to cytoskeletal filaments. Conclusion: We could show that PELO is subcellularly localized at the actin cytoskeleton, interacts with HAX1, EIF3G and SRPX proteins and that this interaction occurs at the cytoskeleton. Binding of PELO to cytoskeleton-associated proteins may facilitate PELO to detect and degrade aberrant mRNAs, at which the ribosome is stalled during translation."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Ad 129/2-1, 2]"],["dc.identifier.doi","10.1186/1471-2121-11-28"],["dc.identifier.isi","000277848800001"],["dc.identifier.pmid","20406461"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5678"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20108"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2121"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Pelota interacts with HAX1, EIF3G and SRPX and the resulting protein complexes are associated with the actin cytoskeleton"],["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.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Kurz, Kathrin"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:24:12Z"],["dc.date.available","2018-11-07T11:24:12Z"],["dc.date.issued","2009"],["dc.format.extent","E15"],["dc.identifier.isi","000270150800039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56352"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","Basic Cardiovascular Sciences Conference 2009"],["dc.relation.eventlocation","Lake Las Vegas, Henderson, NV"],["dc.relation.issn","0009-7330"],["dc.title","Impedes Mitogenic Signal Propagation (IMP) Is Essential for Embryonic Heart and Brain Development and Controls Cardiac Performance via MAPK Signaling in Vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Pfoertner, Ramona"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Wegner, Christiane"],["dc.date.accessioned","2018-11-07T09:02:17Z"],["dc.date.available","2018-11-07T09:02:17Z"],["dc.date.issued","2012"],["dc.format.extent","172"],["dc.identifier.isi","000312764800462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24647"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","11th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","0165-5728"],["dc.title","Laquinimod reduces astrocytic NF kappa B activation in vitro and in vivo"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1308"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1319"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Menken, Lena"],["dc.contributor.author","Pförtner, Ramona"],["dc.contributor.author","Schmid, Susanne N."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2020-12-10T14:06:33Z"],["dc.date.available","2020-12-10T14:06:33Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/glia.23605"],["dc.identifier.issn","0894-1491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69943"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.issn","0894-1491"],["dc.title","Glial fibrillary acidic protein expression alters astrocytic chemokine release and protects mice from cuprizone-induced demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schmidt, Albrecht"],["dc.contributor.author","Kurz, Kathrin"],["dc.contributor.author","Knoell, Ralph"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Guan-Schmidt, Kaomei"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:09:54Z"],["dc.date.available","2018-11-07T11:09:54Z"],["dc.date.issued","2008"],["dc.format.extent","S423"],["dc.identifier.isi","000262104500692"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53102"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Impedes Mitogenic Signal Propagation (IMP) Is Essential for Embryonic Development and Controls Cardiac Size and Function via MAPK"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2073"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Brain: A Journal of Neurology"],["dc.bibliographiccitation.lastpage","2088"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Jäckle, Katharina"],["dc.contributor.author","Zeis, Thomas"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Junker, Andreas"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2021-04-14T08:24:16Z"],["dc.date.available","2021-04-14T08:24:16Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/brain/awaa158"],["dc.identifier.pmid","32577755"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81225"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/283"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/29"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | B02: Inflammatory neurodegeneration and repair mechanisms in childhood onset autoimmune and neurometabolic demyelinating CNS disease"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Brück"],["dc.title","Molecular signature of slowly expanding lesions in progressive multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]