Maier, Katharina

[["dc.bibliographiccitation.firstpage","6993"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","7000"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Hobom, M."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Weissert, Robert"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Meyer, Ralf"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:44:18Z"],["dc.date.available","2017-09-07T11:44:18Z"],["dc.date.issued","2003"],["dc.description.abstract","Optic neuritis is one of the most common clinical manifestations of multiple sclerosis ( MS), a chronic inflammatory disease of the CNS. High-dosage methylprednisolone treatment has been established as the standard therapy of acute inflammation of the optic nerve ( ON). The rationale for corticosteroid treatment lies in the antiinflammatory and immunosuppressive properties of these drugs, as shown in experimental autoimmune encephalomyelitis (EAE), the animal model of MS. To investigate the influence of methylprednisolone therapy on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the ON, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Optic neuritis was diagnosed by recording visual evoked potentials, and RGC function was monitored by measuring electroretinograms. Methylprednisolone treatment significantly increased RGC apoptosis during MOG-EAE. By Western blot analysis, we identified the underlying molecular mechanism: a suppression of mitogen-activated protein kinase ( MAPK) phosphorylation, which is a key event in an endogenous neuroprotective pathway. The methylprednisolone-induced inhibition of MAPK phosphorylation was calcium dependent. Hence, we provide evidence for negative effects of steroid treatment on neuronal survival during chronic inflammatory autoimmune disease of the CNS, which should result in a reevaluation of the current therapy regimen."],["dc.identifier.gro","3144072"],["dc.identifier.isi","000184587100004"],["dc.identifier.pmid","12904460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1655"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Methylprednisolone increases neuronal apoptosis during autoimmune CNS inflammation by inhibition of an endogenous neuroprotective pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","375"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","385"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:45:35Z"],["dc.date.available","2017-09-07T11:45:35Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurodegenerative processes determine the clinical disease course of multiple sclerosis, an inflammatory autoimmune CNS disease that frequently manifests with acute optic neuritis. None of the established multiple sclerosis therapies has been shown to clearly reduce neurodegeneration. In a rat model of experimental autoimmune encephalomyelitis, we recently demonstrated increased neuronal apoptosis under methylprednisolone therapy, although CNS inflammation was effectively controlled. In the present study, we combined steroid treatment with application of erythropoietin to target inflammatory as well as neurodegenerative aspects. After immunization with myelin oligodendrocyte glycoprotein (MOG), animals were randomly assigned to six treatment groups receiving different combinations of erythropoietin and methylprednisolone, or respective monotherapies. After MOG-induced experimental autoimmune encephalomyelitis became clinically manifest, optic neuritis was monitored by recording visual evoked potentials. The function of retinal ganglion cells, the neurons that form the axons of the optic nerve, was measured by electroretinograms. Functional and histo pathological data of retinal ganglion cells and optic nerves revealed that neuron and axon protection was most effective when erythropoietin treatment that was started at immunization was combined with high-dose methylprednisolone therapy given from days 1 to 3 of MOG-induced experimental autoimmune encephalomyelitis. In contrast, isolated neuronal or axonal protection without clinical benefit was achieved under monotherapy with erythropoietin or methylprednisolone, respectively."],["dc.identifier.doi","10.1093/brain/awh365"],["dc.identifier.gro","3150407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7168"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.doi","10.1093/brain/awh365"],["dc.relation.issn","0006-8950"],["dc.title","Combined therapy with methylprednisolone and erythropoietin in a model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain pathology"],["dc.bibliographiccitation.lastpage","157"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Hobom, M."],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Weisser, R"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Radhakrishnan, A."],["dc.contributor.author","Krämer, Bernd"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:43:58Z"],["dc.date.available","2017-09-07T11:43:58Z"],["dc.date.issued","2004"],["dc.description.abstract","Neuronal and axonal damage is considered to be the main cause for long-term disability in multiple sclerosis. We analyzed the mechanisms and kinetics of neuronal cell death in experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) by combining an electrophysiological in vivo assessment of the optic pathway with the investigation of retinal ganglion cell (RGC) counts. In accordance with our previous findings in this animal model, neuritis of the optic nerve (ON) leads to apoptotic RGC death. By further investigating the time course of RGC apoptosis in the present study, we found that neuronal cell death together with decreased visual acuity values occurred before the onset of clinical symptoms. Simultaneously with the time course of RGC apoptosis, we found a down-regulation of phospho-Akt as well as a shift in the relation of 2 proteins of the Bcl-2 family Bax and Bcl-2, towards a more proapoptotic ratio in these cells. Comparing the kinetics and mechanisms of RGC death during MOG-EAE with those following complete surgical transection of the ON, we found significant agreement. We hypothesize that the main reason for RGC loss in MOG-EAE is the inflammatory attack but RGC death also occurs independently of histopathological ON changes."],["dc.identifier.doi","10.1111/j.1750-3639.2004.tb00047.x"],["dc.identifier.gro","3143999"],["dc.identifier.isi","000221410900004"],["dc.identifier.pmid","15193027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1575"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1015-6305"],["dc.relation.issn","1015-6305"],["dc.title","Mechanisms and time course of neuronal degeneration in experimental autoimmune encephalomyelitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","514"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","525"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Maier, K."],["dc.contributor.author","Merkler, D."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Taheri, N."],["dc.contributor.author","Kuhnert, A. V."],["dc.contributor.author","Williams, S. K."],["dc.contributor.author","Neusch, C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:49:51Z"],["dc.date.available","2017-09-07T11:49:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Axonal destruction and neuronal loss occur early during multiple sclerosis, an autoimmune inflammatory CNS disease that frequently manifests with acute optic neuritis. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of minocycline on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials and RGC function was monitored by measuring electroretinograms. Functional and histopathological data of RGCs and optic nerves revealed neuronal and axonal protection when minocycline treatment was started on the day of immunization. Furthermore, we demonstrate that minocycline-induced neuroprotection is related to a direct antagonism of multiple mechanisms leading to neuronal cell death such as the induction of anti-apoptotic intracellular signalling pathways and a decrease in glutamate excitotoxicity. From these observations, we conclude that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties. This hypothesis was confirmed in a non-inflammatory disease model leading to degeneration of RGCs, the surgical transection of the optic nerve. (c) 2007 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.nbd.2006.10.022"],["dc.identifier.gro","3143534"],["dc.identifier.isi","000244872200007"],["dc.identifier.pmid","17239606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1059"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0969-9961"],["dc.title","Multiple neuroprotective mechanisms of minocycline in autoimmune CNS inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","378"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Brain pathology"],["dc.bibliographiccitation.lastpage","387"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Rau, Christian R."],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Weissert, Robert"],["dc.contributor.author","Taheri, Naimeh"],["dc.contributor.author","Kuhnert, Antje V."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:43:14Z"],["dc.date.available","2017-09-07T11:43:14Z"],["dc.date.issued","2004"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the CNS which leads to demyelination, axonal destruction and neuronal loss in the early stages. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of ciliary neurotrophic factor (CNTF) on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve, we used a rat model of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials, and RGC function was monitored by measuring electroretinograms. This study demonstrates that CNTF has a neuroprotective effect on affected RGCs during acute optic neuritis. Furthermore, we demonstrate that CNTF exerts its neuroprotective effect through activation of the Janus kinase/signal transducer and activator of transcription pathway, mitogen activated protein kinases and a shift in the Bcl-2 family of proteins towards the anti-apoptotic side. In summary, our results demonstrate that CNTF can serve as an effective neuroprotective treatment in a rat model of MS that especially reflects the neurodegenerative aspects of this disease."],["dc.identifier.doi","10.1111/j.1750-3639.2004.tb00081.x"],["dc.identifier.isi","000225174100006"],["dc.identifier.pmid","15605985"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1508"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1015-6305"],["dc.relation.issn","1015-6305"],["dc.title","Ciliary neurotrophic factor protects retinal ganglion cells from secondary cell death during acute autoimmune optic neuritis in rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","172"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","181"],["dc.bibliographiccitation.volume","201"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:52:35Z"],["dc.date.available","2017-09-07T11:52:35Z"],["dc.date.issued","2006"],["dc.description.abstract","lntcrferon-beta-1a (IFN-beta-1a) is an approved treatment for multiple sclerosis (MS). It improves the disease course by reducing the relapse rate as well as the persistent neurological deficits. Recent MRI and post-mortem studies revealed that neuronal and axonal damage are most relevant for chronic disability in MS patients. We have characterized previously time course and mechanisms of neuronal apoptosis in a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis. In this animal model, application of IFN-beta-1a three times per week slightly decreases the loss of retinal ganglion cells (RGCs), the neurons that form the axons within the optic nerve. In contrast to neurotrophic factors, this cytokine does not directly protect cultured RGCs from apoptosis. We conclude that IFN-beta-1a is a suitable candidate to be combined with a directly neuroprotective agent in order to further decrease axonal and neuronal degeneration in MS patients. (c) 2006 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2006.04.015"],["dc.identifier.gro","3143633"],["dc.identifier.isi","000240152100019"],["dc.identifier.pmid","16764858"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1169"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0014-4886"],["dc.subject","EAE; interferon-beta; Neuronal apoptosis; Retinal ganglion cells; Mitogen-activated protein kinase; Axonal damage"],["dc.title","Effects of interferon-beta-1a on neuronal survival under autoimmune inflammatory conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1353"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","1364"],["dc.bibliographiccitation.volume","169"],["dc.contributor.author","Maier, K."],["dc.contributor.author","Kuhnert, A. V."],["dc.contributor.author","Taheri, N."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Storch, M. K."],["dc.contributor.author","Williams, S. K."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:52:29Z"],["dc.date.available","2017-09-07T11:52:29Z"],["dc.date.issued","2006"],["dc.description.abstract","Axonal destruction and neuronal loss occur early during multiple sclerosis (MS), an autoimmune inflammatory central nervous system disease that frequently manifests with acute optic neuritis. Glatiramer acetate (GA) and interferon-beta-1b (IFN-beta-1b) are two immunomodulatory agents that have been shown to decrease the frequency of MS relapses. However, the question of whether these substances can slow neurodegeneration in MS patients is the subject of controversy. In a rat model of experimental autoimmune encephalomyelitis, we investigated the effects of GA and IFN-beta-1b on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. For each substance, therapy was, started 14 days before immunization, on the day of immunization, or on the day of clinical disease onset. After myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis became clinically manifest, optic neuritis was monitored by recording visual evoked potentials. The function of RGCs was measured by electroretinograms. Although early GA or IFN-beta-1b treatment showed benefit on disease activity, only treatment with GA exerted protective effects on RGCs, as revealed by measuring neurodegeneration and neuronal function. Furthermore, we demonstrate that this GA-induced neuroprotection does not exclusively depend on the reduction of inflammatory infiltrates within the optic nerve."],["dc.identifier.doi","10.2353/ajpath.2006.060159"],["dc.identifier.gro","3143616"],["dc.identifier.isi","000240872400023"],["dc.identifier.pmid","17003491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1150"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0002-9440"],["dc.title","Effects of glatiramer acetate and interferon-beta on neurodegeneration in a model of multiple sclerosis: A comparative study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S181"],["dc.bibliographiccitation.issue","Suppl. 2"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","S192"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2004"],["dc.description.abstract","In multiple sclerosis (MS), long-term disability is primarily caused by axonal and neuronal damage. We demonstrated in a previous study that neuronal apoptosis occurs early during experimental autoimmune encephalomyelitis, a common animal model of MS. In the present study, we show that, in rats suffering from myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis, systemic application of erythropoietin (Epo) significantly increased survival and function of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. We identified three independent intracellular signaling pathways involved in Epo-induced neuroprotection in vivo: Protein levels of phospho-Akt, phospho-MAPK 1 and 2, and Bcl-2 were increased under Epo application. Using a combined treatment of Epo together with a selective inhibitor of phosphatidylinositol 3-kinase (PI3-K) prevented upregulation of phospho-Akt and consecutive RGC rescue. We conclude that in MOG-EAE the PI3-K/Akt pathway has an important influence on RGC survival under systemic treatment with Epo."],["dc.identifier.doi","10.1038/sj.cdd.4401504"],["dc.identifier.gro","3150406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7167"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1350-9047"],["dc.subject","optic neuritis; erythropoietin; retinal ganglion cells; Bcl-2 family; phosphatidylinositol 3-kinase"],["dc.title","Neuroprotective effects and intracellular signaling pathways of erythropoietin in a rat model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","458"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Molecular Systems Biology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Miller, C."],["dc.contributor.author","Schwalb, B."],["dc.contributor.author","Maier, K."],["dc.contributor.author","Schulz, D."],["dc.contributor.author","Duemcke, S."],["dc.contributor.author","Zacher, B."],["dc.contributor.author","Mayer, A."],["dc.contributor.author","Sydow, J."],["dc.contributor.author","Marcinowski, L."],["dc.contributor.author","Doelken, L."],["dc.contributor.author","Martin, D. E."],["dc.contributor.author","Tresch, A."],["dc.contributor.author","Cramer, P."],["dc.date.accessioned","2017-09-07T11:44:22Z"],["dc.date.available","2017-09-07T11:44:22Z"],["dc.date.issued","2011"],["dc.description.abstract","To obtain rates of mRNA synthesis and decay in yeast, we established dynamic transcriptome analysis (DTA). DTA combines non‐perturbing metabolic RNA labeling with dynamic kinetic modeling. DTA reveals that most mRNA synthesis rates are around several transcripts per cell and cell cycle, and most mRNA half‐lives range around a median of 11 min. DTA can monitor the cellular response to osmotic stress with higher sensitivity and temporal resolution than standard transcriptomics. In contrast to monotonically increasing total mRNA levels, DTA reveals three phases of the stress response. During the initial shock phase, mRNA synthesis and decay rates decrease globally, resulting in mRNA storage. During the subsequent induction phase, both rates increase for a subset of genes, resulting in production and rapid removal of stress‐responsive mRNAs. During the recovery phase, decay rates are largely restored, whereas synthesis rates remain altered, apparently enabling growth at high salt concentration. Stress‐induced changes in mRNA synthesis rates are predicted from gene occupancy with RNA polymerase II. DTA‐derived mRNA synthesis rates identified 16 stress‐specific pairs/triples of cooperative transcription factors, of which seven were known. Thus, DTA realistically monitors the dynamics in mRNA metabolism that underlie gene regulatory systems."],["dc.identifier.doi","10.1038/msb.2010.112"],["dc.identifier.gro","3142788"],["dc.identifier.isi","000287095100003"],["dc.identifier.pmid","21206491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/230"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1744-4292"],["dc.title","Dynamic transcriptome analysis measures rates of mRNA synthesis and decay in yeast"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","218"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","226"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Taheri, Naimeh"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.contributor.author","Kuhnert, Antje V."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Gadjanski, L."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:54:11Z"],["dc.date.available","2017-09-07T11:54:11Z"],["dc.date.issued","2005"],["dc.description.abstract","In multiple sclerosis (MS), post-mortem studies of human brain tissue as well as data from animal models have shown that apoptosis of neurons occurs to a significant extent during this disease. As neurodegeneration in MS correlates with permanent neurological deficits in patients, understanding the mechanisms would be an important precondition for designing appropriate neuroprotective therapies. Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis often affects the optic nerve and leads to consecutive apoptosis of retinal ganglion cells (RGCs), the neurons that form its axons. In this study, we fused Bcl-X-L to the protein transduction domain of the HIV-transactivator of transcription. Thereby, this antiapoptotic member of the Bcl-2 family was delivered into RGCs of rats with electrophysiologically diagnosed optic neuritis. Transduction of Bel-XI, in our study led to significant rescue of RGCs indicating the relevance of this pathway for neuronal survival under autoimmune inflammatory conditions. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.nbd.2005.03.003"],["dc.identifier.gro","3143794"],["dc.identifier.isi","000233096700005"],["dc.identifier.pmid","16242630"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1348"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0969-9961"],["dc.title","HIV-tat-mediated BCl-X-L delivery protects retinal ganglion cells during experimental autoimmune optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]