Kirchhoff, Frank

[["dc.bibliographiccitation.artnumber","1371"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.lastpage","16"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Joas, Simone"],["dc.contributor.author","Parrish, Erica H."],["dc.contributor.author","Gnanadurai, Clement W."],["dc.contributor.author","Lump, Edina"],["dc.contributor.author","Stürzel, Christina M."],["dc.contributor.author","Parrish, Nicholas F."],["dc.contributor.author","Learn, Gerald H."],["dc.contributor.author","Sauermann, Ulrike"],["dc.contributor.author","Neumann, Berit"],["dc.contributor.author","Rensing, Kerstin Mätz"],["dc.contributor.author","Fuchs, Dietmar"],["dc.contributor.author","Billingsley, James M."],["dc.contributor.author","Bosinger, Steven E."],["dc.contributor.author","Silvestri, Guido"],["dc.contributor.author","Apetrei, Cristian"],["dc.contributor.author","Huot, Nicolas"],["dc.contributor.author","Garcia-Tellez, Thalia"],["dc.contributor.author","Müller-Trutwin, Michaela"],["dc.contributor.author","Hotter, Dominik"],["dc.contributor.author","Sauter, Daniel"],["dc.contributor.author","Stahl-Hennig, Christiane"],["dc.contributor.author","Hahn, Beatrice H."],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2018-11-15T12:52:42Z"],["dc.date.accessioned","2021-10-27T13:13:05Z"],["dc.date.available","2018-11-15T12:52:42Z"],["dc.date.available","2021-10-27T13:13:05Z"],["dc.date.issued","2018"],["dc.description.abstract","HIV-1 causes chronic inflammation and AIDS in humans, whereas related simian immunodeficiency viruses (SIVs) replicate efficiently in their natural hosts without causing disease. It is currently unknown to what extent virus-specific properties are responsible for these different clinical outcomes. Here, we incorporate two putative HIV-1 virulence determinants, i.e., a Vpu protein that antagonizes tetherin and blocks NF-κB activation and a Nef protein that fails to suppress T cell activation via downmodulation of CD3, into a non-pathogenic SIVagm strain and test their impact on viral replication and pathogenicity in African green monkeys. Despite sustained high-level viremia over more than 4 years, moderately increased immune activation and transcriptional signatures of inflammation, the HIV-1-like SIVagm does not cause immunodeficiency or any other disease. These data indicate that species-specific host factors rather than intrinsic viral virulence factors determine the pathogenicity of primate lentiviruses."],["dc.identifier.doi","10.1038/s41467-018-03762-3"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91749"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2041-1723"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Species-specific host factors rather than virus-intrinsic virulence determine primate lentiviral pathogenicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3791"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.lastpage","3800"],["dc.bibliographiccitation.volume","96"],["dc.contributor.author","Neher, Richard A."],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neher, Erwin"],["dc.contributor.author","Theis, Fabian J."],["dc.contributor.author","Zeug, Andre"],["dc.date.accessioned","2018-11-07T08:30:00Z"],["dc.date.available","2018-11-07T08:30:00Z"],["dc.date.issued","2009"],["dc.description.abstract","Methods of blind source separation are used in many contexts to separate composite data sets according to their sources. Multiply labeled fluorescence microscopy images represent such sets, in which the sources are the individual labels. Then distributions are the quantities of interest and have to be extracted from the images. This is often challenging, since the recorded emission spectra of fluorescent dyes are environment- and instrument-specific. We have developed a nonnegative matrix factorization (NMF) algorithm to detect and separate spectrally distinct components of multiply labeled fluorescence images. It operates on spectrally resolved images and delivers both the emission spectra of the identified components and images of their abundance. We tested the proposed method using biological samples labeled with up to four spectrally overlapping fluorescent labels. In most cases, NMF accurately decomposed the images into contributions of individual dyes. However, the Solutions are not unique when spectra overlap strongly or when images are diffuse in their structure. To arrive at satisfactory results in such cases, we extended NMF to incorporate preexisting qualitative knowledge about spectra and label distributions. We show how data acquired through excitations at two or three different wavelengths can be integrated and that multiple excitations greatly facilitate the decomposition. By allowing reliable decomposition in cases where the spectra of the individual labels are not known or are known only inaccurately, the proposed algorithms greatly extend the range of questions that can be addressed with quantitative microscopy."],["dc.identifier.doi","10.1016/j.bpj.2008.10.068"],["dc.identifier.isi","000266397700033"],["dc.identifier.pmid","19413985"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7763"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16787"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","0006-3495"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Blind Source Separation Techniques for the Decomposition of Multiply Labeled Fluorescence Images"],["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","e17910"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Nadrigny, Fabien"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2018-11-07T08:58:04Z"],["dc.date.available","2018-11-07T08:58:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Mutations in the enzyme superoxide dismutase-1 (SOD1) cause hereditary variants of the fatal motor neuronal disease Amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous: neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring non-neuronal cells. In vivo imaging by two-photon laser-scanning microscopy was used to compare the role of microglia/macrophage-related neuroinflammation in the CNS and PNS using ALS-linked transgenic SOD1(G93A) mice. These mice contained labeled projection neurons and labeled microglia/macrophages. In the affected lateral spinal cord (in contrast to non-affected dorsal columns), different phases of microglia-mediated inflammation were observed: highly reactive microglial cells in preclinical stages (in 60-day-old mice the reaction to axonal transection was similar to 180% of control) and morphologically transformed microglia that have lost their function of tissue surveillance and injury-directed response in clinical stages (reaction to axonal transection was lower than 50% of control). Furthermore, unlike CNS microglia, macrophages of the PNS lack any substantial morphological reaction while preclinical degeneration of peripheral motor axons and neuromuscular junctions was observed. We present in vivo evidence for a different inflammatory activity of microglia and macrophages: an aberrant neuroinflammatory response of microglia in the CNS and an apparently mainly neurodegenerative process in the PNS."],["dc.identifier.doi","10.1371/journal.pone.0017910"],["dc.identifier.isi","000288545100043"],["dc.identifier.pmid","21437247"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23554"],["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 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","In Vivo Imaging Reveals Distinct Inflammatory Activity of CNS Microglia versus PNS Macrophages in a Mouse Model for ALS"],["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","e43963"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PlosOne"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Zschüntzsch, Jana"],["dc.contributor.author","Steffens, Heinz"],["dc.contributor.author","Scheffel, Jörg"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Le Meur, Karim"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Schomburg, Eike D."],["dc.contributor.author","Neusch, Clemens"],["dc.date.accessioned","2019-07-09T11:53:39Z"],["dc.date.available","2019-07-09T11:53:39Z"],["dc.date.issued","2012"],["dc.description.abstract","Mutations in SOD1 cause hereditary variants of the fatal motor neuron disease amyotrophic lateral sclerosis (ALS). Pathophysiology of the disease is non-cell-autonomous, with toxicity deriving also from glia. In particular, microglia contribute to disease progression. Methylene blue (MB) inhibits the effect of nitric oxide, which mediates microglial responses to injury. In vivo 2P-LSM imaging was performed in ALS-linked transgenic SOD1G93A mice to investigate the effect of MB on microglia-mediated inflammation in the spinal cord. Local superfusion of the lateral spinal cord with MB inhibited the microglial reaction directed at a laser-induced axon transection in control and SOD1G93A mice. In vitro, MB at high concentrations inhibited cytokine and chemokine release from microglia of control and advanced clinical SOD1G93A mice. Systemic MB-treatment of SOD1G93A mice at early preclinical stages significantly delayed disease onset and motor dysfunction. However, an increase of MB dose had no additional effect on disease progression; this was unexpected in view of the local anti-inflammatory effects. Furthermore, in vivo imaging of systemically MB-treated mice also showed no alterations of microglia activity in response to local lesions. Thus although systemic MB treatment had no effect on microgliosis, instead, its use revealed an important influence on motor neuron survival as indicated by an increased number of lumbar anterior horn neurons present at the time of disease onset. Thus, potentially beneficial effects of locally applied MB on inflammatory events contributing to disease progression could not be reproduced in SOD1G93A mice via systemic administration, whereas systemic MB application delayed disease onset via neuroprotection."],["dc.format.extent","13"],["dc.identifier.doi","10.1371/journal.phone.0043963"],["dc.identifier.fs","592827"],["dc.identifier.pmid","22952827"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7861"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60471"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Influence of Methylene Blue on Microglia-Induced Inflammation and Motor Neuron Degeneration in the SOD1G93A Model for ALS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2104.e10"],["dc.bibliographiccitation.firstpage","2092"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Braun, Elisabeth"],["dc.contributor.author","Hotter, Dominik"],["dc.contributor.author","Koepke, Lennart"],["dc.contributor.author","Zech, Fabian"],["dc.contributor.author","Groß, Rüdiger"],["dc.contributor.author","Sparrer, Konstantin M.J."],["dc.contributor.author","Müller, Janis A."],["dc.contributor.author","Pfaller, Christian K."],["dc.contributor.author","Heusinger, Elena"],["dc.contributor.author","Wombacher, Rebecka"],["dc.contributor.author","Sutter, Kathrin"],["dc.contributor.author","Dittmer, Ulf"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Simmons, Graham"],["dc.contributor.author","Jakobsen, Martin R."],["dc.contributor.author","Conzelmann, Karl-Klaus"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Münch, Jan"],["dc.contributor.author","Fackler, Oliver T."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Sauter, Daniel"],["dc.date.accessioned","2019-07-09T11:51:46Z"],["dc.date.available","2019-07-09T11:51:46Z"],["dc.date.issued","2019"],["dc.description.abstract","Guanylate-binding protein (GBP) 5 is an interferon (IFN)-inducible cellular factor reducing HIV-1 infectivity by an incompletely understood mechanism. Here, we show that this activity is shared by GBP2, but not by other members of the human GBP family. GBP2/5 decrease the activity of the cellular proprotein convertase furin, which mediates conversion of the HIV-1 envelope protein (Env) precursor gp160 into mature gp120 and gp41. Because this process primes HIV-1 Env for membrane fusion, viral particles produced in the presence of GBP2/5 are poorly infectious due to increased incorporation of non-functional gp160. Furin activity is critical for the processing of envelope glycoproteins of many viral pathogens. Consistently, GBP2/5 also inhibit Zika, measles, and influenza A virus replication and decrease infectivity of viral particles carrying glycoproteins of Marburg and murine leukemia viruses. Collectively, our results show that GPB2/5 exert broad antiviral activity by suppressing the activity of the virus-dependency factor furin."],["dc.identifier.doi","10.1016/j.celrep.2019.04.063"],["dc.identifier.pmid","31091448"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16188"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60006"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","599"],["dc.title","Guanylate-Binding Proteins 2 and 5 Exert Broad Antiviral Activity by Inhibiting Furin-Mediated Processing of Viral Envelope Proteins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","882918"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Seidel, Alina; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Zanoni, Michelle; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Groß, Rüdiger; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Krnavek, Daniela; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Erdemci-Evin, Sümeyye; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","von Maltitz, Pascal; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Albers, Dan P. J.; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Conzelmann, Carina; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Liu, Sichen; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Weil, Tatjana; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Mayer, Benjamin; \n2\nInstitute for Epidemiology and Medical Biometry, Ulm University, Ulm, Germany"],["dc.contributor.affiliation","Hoffmann, Markus; \n3\nInfection Biology Unit, German Primate Center – Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Pöhlmann, Stefan; \n3\nInfection Biology Unit, German Primate Center – Leibniz Institute for Primate Research, Göttingen, Germany"],["dc.contributor.affiliation","Beil, Alexandra; \n5\nCentral Department for Clinical Chemistry, University Hospital Ulm, Ulm, Germany"],["dc.contributor.affiliation","Kroschel, Joris; \n5\nCentral Department for Clinical Chemistry, University Hospital Ulm, Ulm, Germany"],["dc.contributor.affiliation","Kirchhoff, Frank; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Münch, Jan; \n1\nInstitute of Molecular Virology, Ulm University Medical Center, Ulm, Germany"],["dc.contributor.affiliation","Müller, Janis A.; \n7\nInstitute of Virology, Philipps University of Marburg, Marburg, Germany"],["dc.contributor.author","Seidel, Alina"],["dc.contributor.author","Zanoni, Michelle"],["dc.contributor.author","Groß, Rüdiger"],["dc.contributor.author","Krnavek, Daniela"],["dc.contributor.author","Erdemci-Evin, Sümeyye"],["dc.contributor.author","von Maltitz, Pascal"],["dc.contributor.author","Albers, Dan P. J."],["dc.contributor.author","Conzelmann, Carina"],["dc.contributor.author","Liu, Sichen"],["dc.contributor.author","Weil, Tatjana"],["dc.contributor.author","Mayer, Benjamin"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Beil, Alexandra"],["dc.contributor.author","Kroschel, Joris"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Münch, Jan"],["dc.contributor.author","Müller, Janis A."],["dc.date.accessioned","2022-08-09T06:28:09Z"],["dc.date.available","2022-08-09T06:28:09Z"],["dc.date.issued","2022-07-25"],["dc.date.updated","2022-08-08T06:43:11Z"],["dc.description.abstract","In light of the decreasing immune protection against symptomatic SARS-CoV-2 infection after initial vaccinations and the now dominant immune-evasive Omicron variants, ‘booster’ vaccinations are regularly performed to restore immune responses. Many individuals have received a primary heterologous prime-boost vaccination with long intervals between vaccinations, but the resulting long-term immunity and the effects of a subsequent ‘booster’, particularly against Omicron BA.1, have not been defined. We followed a cohort of 23 young adults, who received a primary heterologous ChAdOx1 nCoV-19 BNT162b2 prime-boost vaccination, over a 7-month period and analysed how they responded to a BNT162b2 ‘booster’. We show that already after the primary heterologous vaccination, neutralization titers against Omicron BA.1 are recognizable but that humoral and cellular immunity wanes over the course of half a year. Residual responsive memory T cells recognized spike epitopes of the early SARS-CoV-2 B.1 strain as well as the Delta and BA.1 variants of concern (VOCs). However, the remaining antibody titers hardly neutralized these VOCs. The ‘booster’ vaccination was well tolerated and elicited both high antibody titers and increased memory T cell responses against SARS-CoV-2 including BA.1. Strikingly, in this young heterologously vaccinated cohort the neutralizing activity after the ‘booster’ was almost as potent against BA.1 as against the early B.1 strain. Our results suggest that a ‘booster’ after heterologous vaccination results in effective immune maturation and potent protection against the Omicron BA.1 variant in young adults."],["dc.identifier.doi","10.3389/fimmu.2022.882918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112665"],["dc.language.iso","en"],["dc.relation.eissn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","BNT162b2 booster after heterologous prime-boost vaccination induces potent neutralizing antibodies and T cell reactivity against SARS-CoV-2 Omicron BA.1 in young adults"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e43337"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Bertram, Stephanie"],["dc.contributor.author","Gnirß, Kerstin"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Gawanbacht, Ali"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Ehrhardt, Christina"],["dc.contributor.author","Ludwig, Stephan"],["dc.contributor.author","Kiene, Miriam"],["dc.contributor.author","Moldenhauer, Anna-Sophie"],["dc.contributor.author","Goedecke, Ulrike"],["dc.contributor.author","Karsten, Christina B."],["dc.contributor.author","Kühl, Annika"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2019-07-09T11:53:44Z"],["dc.date.available","2019-07-09T11:53:44Z"],["dc.date.issued","2012"],["dc.description.abstract","The interferon-induced host cell factor tetherin inhibits release of human immunodeficiency virus (HIV) from the plasma membrane of infected cells and is counteracted by the HIV-1 protein Vpu. Influenza A virus (FLUAV) also buds from the plasma membrane and is not inhibited by tetherin. Here, we investigated if FLUAV encodes a functional equivalent of Vpu for tetherin antagonism. We found that expression of the FLUAV protein NS1, which antagonizes the interferon (IFN) response, did not block the tetherin-mediated restriction of HIV release, which was rescued by Vpu. Similarly, tetherinmediated inhibition of HIV release was not rescued by FLUAV infection. In contrast, FLUAV infection induced tetherin expression on target cells in an IFN-dependent manner. These results suggest that FLUAV escapes the antiviral effects of tetherin without encoding a tetherin antagonist with Vpu-like activity."],["dc.identifier.doi","10.1371/journal.pone.0043337"],["dc.identifier.fs","588509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60484"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Influenza A Virus Does Not Encode a Tetherin Antagonist with Vpu-Like Activity and Induces IFN-Dependent Tetherin Expression in Infected Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e4286"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Scheller, Anja"],["dc.contributor.author","Hirrlinger, Petra G."],["dc.contributor.author","Kellert, Beate"],["dc.contributor.author","Tang, Wannan"],["dc.contributor.author","Wehr, Michael C."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Reichenbach, Andreas"],["dc.contributor.author","Sprengel, Rolf"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2019-07-09T11:53:56Z"],["dc.date.available","2019-07-09T11:53:56Z"],["dc.date.issued","2009-01-27"],["dc.description.abstract","Cre/LoxP recombination is the gold standard for conditional gene regulation in mice in vivo. However, promoters driving the expression of Cre recombinase are often active in a wide range of cell types and therefore unsuited to target more specific subsets of cells. To overcome this limitation, we designed inactive ‘‘split-Cre’’ fragments that regain Cre activity when overlapping co-expression is controlled by two different promoters. Using transgenic mice and virus-mediated expression of split-Cre, we show that efficient reporter gene activation is achieved in vivo. In the brain of transgenic mice, we genetically defined a subgroup of glial progenitor cells in which the Plp1- and the Gfap-promoter are simultaneously active, giving rise to both astrocytes and NG2-positive glia. Similarly, a subset of interneurons was labelled after viral transfection using Gad67- and Cck1 promoters to express split-Cre. Thus, split-Cre mediated genomic recombination constitutes a powerful spatial and temporal coincidence detector for in vivo targeting."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0004286"],["dc.identifier.pmid","19172189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8268"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60531"],["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","Split-Cre Complementation Indicates Coincident Activity of Different Genes In Vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1"],["dc.bibliographiccitation.journal","Retrovirology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Koppensteiner, Herwig"],["dc.contributor.author","Höhne, Kristin"],["dc.contributor.author","Gondim, Marcos Vinicius"],["dc.contributor.author","Gobert, Francois-Xavier"],["dc.contributor.author","Widder, Miriam"],["dc.contributor.author","Gundlach, Swantje"],["dc.contributor.author","Heigele, Anke"],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Benaroch, Philippe"],["dc.contributor.author","Schindler, Michael"],["dc.date.accessioned","2019-07-09T11:41:19Z"],["dc.date.available","2019-07-09T11:41:19Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: Increased cellular iron levels are associated with high mortality in HIV-1 infection. Moreover iron is an important cofactor for viral replication, raising the question whether highly divergent lentiviruses actively modulate iron homeostasis. Here, we evaluated the effect on cellular iron uptake upon expression of the accessory protein Nef from different lentiviral strains. RESULTS: Surface Transferrin receptor (TfR) levels are unaffected by Nef proteins of HIV-1 and its simian precursors but elevated in cells expressing Nefs from most other primate lentiviruses due to reduced TfR internalization. The SIV Nef-mediated reduction of TfR endocytosis is dependent on an N-terminal AP2 binding motif that is not required for downmodulation of CD4, CD28, CD3 or MHCI. Importantly, SIV Nef-induced inhibition of TfR endocytosis leads to the reduction of Transferrin uptake and intracellular iron concentration and is accompanied by attenuated lentiviral replication in macrophages. CONCLUSION: Inhibition of Transferrin and thereby iron uptake by SIV Nef might limit viral replication in myeloid cells. Furthermore, this new SIV Nef function could represent a virus-host adaptation that evolved in natural SIV-infected monkeys."],["dc.identifier.doi","10.1186/1742-4690-11-1"],["dc.identifier.pmid","24383984"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58399"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1742-4690"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Endocytosis"],["dc.subject.mesh","Gene Products, nef"],["dc.subject.mesh","Haplorhini"],["dc.subject.mesh","Iron"],["dc.subject.mesh","Receptors, Transferrin"],["dc.subject.mesh","Simian immunodeficiency virus"],["dc.subject.mesh","Transferrin"],["dc.title","Lentiviral Nef suppresses iron uptake in a strain specific manner through inhibition of Transferrin endocytosis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1001604"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Fruehbeis, Carsten"],["dc.contributor.author","Froehlich, Dominik"],["dc.contributor.author","Kuo, Wen Ping"],["dc.contributor.author","Amphornrat, Jesa"],["dc.contributor.author","Thilemann, Sebastian"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Klugmann, Matthias"],["dc.contributor.author","Trotter, Jacqueline"],["dc.contributor.author","Kraemer-Albers, Eva-Maria"],["dc.date.accessioned","2018-11-07T09:22:56Z"],["dc.date.available","2018-11-07T09:22:56Z"],["dc.date.issued","2013"],["dc.description.abstract","Reciprocal interactions between neurons and oligodendrocytes are not only crucial for myelination, but also for long-term survival of axons. Degeneration of axons occurs in several human myelin diseases, however the molecular mechanisms of axon-glia communication maintaining axon integrity are poorly understood. Here, we describe the signal-mediated transfer of exosomes from oligodendrocytes to neurons. These endosome-derived vesicles are secreted by oligodendrocytes and carry specific protein and RNA cargo. We show that activity-dependent release of the neurotransmitter glutamate triggers oligodendroglial exosome secretion mediated by Ca2+ entry through oligodendroglial NMDA and AMPA receptors. In turn, neurons internalize the released exosomes by endocytosis. Injection of oligodendroglia-derived exosomes into the mouse brain results in functional retrieval of exosome cargo in neurons. Supply of cultured neurons with oligodendroglial exosomes improves neuronal viability under conditions of cell stress. These findings indicate that oligodendroglial exosomes participate in a novel mode of bidirectional neuron-glia communication contributing to neuronal integrity."],["dc.identifier.doi","10.1371/journal.pbio.1001604"],["dc.identifier.isi","000322592700008"],["dc.identifier.pmid","23874151"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29458"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Neurotransmitter-Triggered Transfer of Exosomes Mediates Oligodendrocyte-Neuron Communication"],["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"]]