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  1. Article ; Online: Helicobacter pylori

    Ralser, Anna / Dietl, Alisa / Jarosch, Sebastian / Engelsberger, Veronika / Wanisch, Andreas / Janssen, Klaus Peter / Middelhoff, Moritz / Vieth, Michael / Quante, Michael / Haller, Dirk / Busch, Dirk H / Deng, Li / Mejías-Luque, Raquel / Gerhard, Markus

    Gut

    2023  Volume 72, Issue 7, Page(s) 1258–1270

    Abstract: Objective: Helicobacter pylori: Design: We infected two : Results: H. pylori: Conclusions: Our studies provide evidence ... ...

    Abstract Objective: Helicobacter pylori
    Design: We infected two
    Results: H. pylori
    Conclusions: Our studies provide evidence that
    MeSH term(s) Humans ; Mice ; Animals ; Helicobacter pylori/genetics ; Helicobacter Infections/complications ; Helicobacter Infections/microbiology ; Mice, Inbred C57BL ; Carcinogenesis/pathology ; Stomach Neoplasms/pathology ; Colonic Neoplasms/pathology ; Microbiota ; Mucus ; Gastric Mucosa/pathology
    Language English
    Publishing date 2023-04-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2022-328075
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  2. Book ; Online ; Thesis: Untersuchungen zur Proteinbiosynthese bei hippokampusabhängigen Lernprozessen der Maus

    Wanisch, Klaus

    2007  

    Author's details von Klaus Wanisch
    Language German
    Size Online-Ressource
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Univ., Diss--München, 2007
    Database Former special subject collection: coastal and deep sea fishing

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  3. Book ; Online ; Thesis: Untersuchungen zur Proteinbiosynthese bei hippokampusabhängigen Lernprozessen der Maus

    Wanisch, Klaus [Verfasser]

    2007  

    Author's details von Klaus Wanisch
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  4. Article ; Online: Tackling obstacles for gene therapy targeting neurons: disrupting perineural nets with hyaluronidase improves transduction.

    Wanisch, Klaus / Kovac, Stjepana / Schorge, Stephanie

    PloS one

    2013  Volume 8, Issue 1, Page(s) e53269

    Abstract: Gene therapy has been proposed for many diseases in the nervous system. In most cases for successful treatment, therapeutic vectors must be able to transduce mature neurons. However, both in vivo, and in vitro, where preliminary characterisation of viral ...

    Abstract Gene therapy has been proposed for many diseases in the nervous system. In most cases for successful treatment, therapeutic vectors must be able to transduce mature neurons. However, both in vivo, and in vitro, where preliminary characterisation of viral particles takes place, transduction of neurons is typically inefficient. One possible explanation is that the extracellular matrix (ECM), forming dense perineural nets (PNNs) around neurons, physically blocks access to the cell surface. We asked whether co-administration of lentiviral vectors with an enzyme that disrupts the ECM could improve transduction efficiency. Using hyaluronidase, an enzyme which degrades hyaluronic acid, a high molecular weight molecule of the ECM with mainly a scaffolding function, we show that in vitro in mixed primary cortical cultures, and also in vivo in rat cortex, hyaluronidase co-administration increased the percentage of transduced mature, NeuN-positive neurons. Moreover, hyaluronidase was effective at doses that showed no toxicity in vitro based on propidium iodide staining of treated cultures. Our data suggest that limited efficacy of neuronal transduction is partly due to PNNs surrounding neurons, and further that co-applying hyaluronidase may benefit applications where efficient transduction of neurons in vitro or in vivo is required.
    MeSH term(s) Animals ; Brain/pathology ; Genetic Therapy/methods ; Genetic Vectors ; HEK293 Cells ; Humans ; Hyaluronoglucosaminidase/pharmacology ; Image Processing, Computer-Assisted ; Lentivirus/metabolism ; Male ; Nerve Net ; Neurogenesis ; Neurons/metabolism ; Primary Cell Culture ; Rats ; Rats, Sprague-Dawley ; Transduction, Genetic
    Chemical Substances Hyaluronoglucosaminidase (EC 3.2.1.35)
    Language English
    Publishing date 2013-01-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0053269
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  5. Article ; Online: Time course and efficiency of protein synthesis inhibition following intracerebral and systemic anisomycin treatment.

    Wanisch, Klaus / Wotjak, Carsten T

    Neurobiology of learning and memory

    2008  Volume 90, Issue 3, Page(s) 485–494

    Abstract: Since its discovery in the 1960s, anisomycin has been used for studying the impact of protein synthesis for manifold cerebral processes such as long-term plastic changes after learning. The common limitation of nearly all pharmacological experiments, ... ...

    Abstract Since its discovery in the 1960s, anisomycin has been used for studying the impact of protein synthesis for manifold cerebral processes such as long-term plastic changes after learning. The common limitation of nearly all pharmacological experiments, including anisomycin treatment, is to precisely verify the affected brain regions. Here we illustrate anisomycin effects on protein synthesis in distinct brain regions of mice (C57BL/6JOlaHsd), revealing differences between three modes of anisomycin application (subcutaneous, s.c.; intraperitoneal, i.p.; local microinfusions into the hippocampus). Our method is based on inhibition of the incorporation of the radioactively-labelled amino acids [(35)S]-Methionine/Cysteine into newly synthesised proteins. Washing the brain slices before autoradiography removes pools of amino acids, which have not been incorporated into newly synthesised proteins, thus, illustrating pure protein synthesis. By comparing different routes of systemic anisomycin application (i.p. versus s.c.; 150 mg/kg) it became evident that the effect of i.p. injection of anisomycin is fully reversed after 6 h, whereas s.c. injection is inhibiting protein synthesis in the hippocampus even 9 h after application. Local microinfusions of anisomycin into the hippocampus were shown to have long-lasting effects as well, which reversed as late as 9 h after injection. The diffusion of anisomycin was maximal at 3 h after injection and more precisely confined to the intended area using a lower dose (20 microg/site) instead of the commonly used dose of 62.5 microg/site. The broad time window of anisomycin action, as revealed in our study, has to be considered, if it comes to the interpretation of time course studies within the context of protein synthesis-dependent processes.
    MeSH term(s) Analysis of Variance ; Animals ; Anisomycin/administration & dosage ; Anisomycin/pharmacokinetics ; Autoradiography ; Dose-Response Relationship, Drug ; Drug Administration Routes ; Hippocampus/drug effects ; Hippocampus/metabolism ; Male ; Memory/drug effects ; Memory/physiology ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/biosynthesis ; Protein Biosynthesis/drug effects ; Protein Synthesis Inhibitors/administration & dosage ; Protein Synthesis Inhibitors/pharmacokinetics ; Time Factors
    Chemical Substances Nerve Tissue Proteins ; Protein Synthesis Inhibitors ; Anisomycin (6C74YM2NGI)
    Language English
    Publishing date 2008-10
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 1223366-3
    ISSN 1095-9564 ; 1074-7427
    ISSN (online) 1095-9564
    ISSN 1074-7427
    DOI 10.1016/j.nlm.2008.02.007
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  6. Article ; Online: Tackling obstacles for gene therapy targeting neurons

    Klaus Wanisch / Stjepana Kovac / Stephanie Schorge

    PLoS ONE, Vol 8, Iss 1, p e

    disrupting perineural nets with hyaluronidase improves transduction.

    2013  Volume 53269

    Abstract: Gene therapy has been proposed for many diseases in the nervous system. In most cases for successful treatment, therapeutic vectors must be able to transduce mature neurons. However, both in vivo, and in vitro, where preliminary characterisation of viral ...

    Abstract Gene therapy has been proposed for many diseases in the nervous system. In most cases for successful treatment, therapeutic vectors must be able to transduce mature neurons. However, both in vivo, and in vitro, where preliminary characterisation of viral particles takes place, transduction of neurons is typically inefficient. One possible explanation is that the extracellular matrix (ECM), forming dense perineural nets (PNNs) around neurons, physically blocks access to the cell surface. We asked whether co-administration of lentiviral vectors with an enzyme that disrupts the ECM could improve transduction efficiency. Using hyaluronidase, an enzyme which degrades hyaluronic acid, a high molecular weight molecule of the ECM with mainly a scaffolding function, we show that in vitro in mixed primary cortical cultures, and also in vivo in rat cortex, hyaluronidase co-administration increased the percentage of transduced mature, NeuN-positive neurons. Moreover, hyaluronidase was effective at doses that showed no toxicity in vitro based on propidium iodide staining of treated cultures. Our data suggest that limited efficacy of neuronal transduction is partly due to PNNs surrounding neurons, and further that co-applying hyaluronidase may benefit applications where efficient transduction of neurons in vitro or in vivo is required.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2013-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Integration-deficient lentiviral vectors: a slow coming of age.

    Wanisch, Klaus / Yáñez-Muñoz, Rafael J

    Molecular therapy : the journal of the American Society of Gene Therapy

    2009  Volume 17, Issue 8, Page(s) 1316–1332

    Abstract: Lentiviral vectors are very efficient at transducing dividing and quiescent cells, which makes them highly useful tools for genetic analysis and gene therapy. Traditionally this efficiency was considered dependent on provirus integration in the host cell ...

    Abstract Lentiviral vectors are very efficient at transducing dividing and quiescent cells, which makes them highly useful tools for genetic analysis and gene therapy. Traditionally this efficiency was considered dependent on provirus integration in the host cell genome; however, recent results have challenged this view. So called integration-deficient lentiviral vectors (IDLVs) can be produced through the use of integrase mutations that specifically prevent proviral integration, resulting in the generation of increased levels of circular vector episomes in transduced cells. These lentiviral episomes lack replication signals and are gradually lost by dilution in dividing cells, but are stable in quiescent cells. Compared to integrating lentivectors, IDLVs have a greatly reduced risk of causing insertional mutagenesis and a lower risk of generating replication-competent recombinants (RCRs). IDLVs can mediate transient gene expression in proliferating cells, stable expression in nondividing cells in vitro and in vivo, specific immune responses, RNA interference, homologous recombination (gene repair, knock-in, and knock-out), site-specific recombination, and transposition. IDLVs can be converted into replicating episomes, suggesting that if a clinically applicable system can be developed they would also become highly appropriate for stable transduction of proliferating tissues in therapeutic applications.
    MeSH term(s) Animals ; Genetic Vectors/genetics ; Humans ; Integrases/genetics ; Lentivirus/genetics ; Mutation ; Transduction, Genetic/methods
    Chemical Substances Integrases (EC 2.7.7.-)
    Language English
    Publishing date 2009-06-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2010592-7
    ISSN 1525-0024 ; 1525-0016
    ISSN (online) 1525-0024
    ISSN 1525-0016
    DOI 10.1038/mt.2009.122
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  8. Article: Long-lasting second stage of recognition memory consolidation in mice.

    Wanisch, Klaus / Wotjak, Carsten T / Engelmann, Mario

    Behavioural brain research

    2008  Volume 186, Issue 2, Page(s) 191–196

    Abstract: We investigated the effects of anisomycin (ANI) treatment (150 mg/kg s.c.) during late stages of memory consolidation in a juvenile recognition task in mice. ANI treatment blocked 24 h recognition memory if administered 9 h, 12 h or 15 h after learning. ... ...

    Abstract We investigated the effects of anisomycin (ANI) treatment (150 mg/kg s.c.) during late stages of memory consolidation in a juvenile recognition task in mice. ANI treatment blocked 24 h recognition memory if administered 9 h, 12 h or 15 h after learning. As shown by a significantly reduced incorporation of radioactively labelled amino acids into newly synthesized proteins, translational arrest by ANI treatment lasted for 3-4 h, thus covering the complete time period between 9 h and 18 h after memory acquisition. Together with previous findings [Richter K, Wolf G, Engelmann M. Social recognition memory requires two stages of protein synthesis in mice. Learn Mem 2005;12(4):407-13], our data suggest two distinct stages of protein synthesis to occur during the first 24 h after learning: an early, relatively short-stage, starting immediately after learning and lasting for approximately 3h, and a second stage starting 6 h after learning lasting for approximately 12 h. This is the first report of such a long-lasting protein synthesis-dependent second consolidation phase in mice and suggests that long-term consolidation of juvenile recognition memory comprises multiple waves of protein synthesis and complex cascades of inter- and intra-cellular signaling processes.
    MeSH term(s) Amino Acids/metabolism ; Animals ; Anisomycin/pharmacology ; Behavior, Animal ; Brain/drug effects ; Brain/metabolism ; Discrimination (Psychology)/drug effects ; Discrimination (Psychology)/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Olfactory Pathways/physiology ; Protein Synthesis Inhibitors/pharmacology ; Recognition (Psychology)/drug effects ; Recognition (Psychology)/physiology ; Smell ; Time Factors
    Chemical Substances Amino Acids ; Protein Synthesis Inhibitors ; Anisomycin (6C74YM2NGI)
    Language English
    Publishing date 2008-01-25
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 449927-x
    ISSN 1872-7549 ; 0166-4328
    ISSN (online) 1872-7549
    ISSN 0166-4328
    DOI 10.1016/j.bbr.2007.08.008
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  9. Article ; Online: Mitochondrial deficits and abnormal mitochondrial retrograde axonal transport play a role in the pathogenesis of mutant Hsp27-induced Charcot Marie Tooth Disease.

    Kalmar, Bernadett / Innes, Amy / Wanisch, Klaus / Kolaszynska, Alicia Koyen / Pandraud, Amelie / Kelly, Gavin / Abramov, Andrey Y / Reilly, Mary M / Schiavo, Giampietro / Greensmith, Linda

    Human molecular genetics

    2017  Volume 26, Issue 17, Page(s) 3313–3326

    Abstract: Mutations in the small heat shock protein Hsp27, encoded by the HSPB1 gene, have been shown to cause Charcot Marie Tooth Disease type 2 (CMT-2) or distal hereditary motor neuropathy (dHMN). Protein aggregation and axonal transport deficits have been ... ...

    Abstract Mutations in the small heat shock protein Hsp27, encoded by the HSPB1 gene, have been shown to cause Charcot Marie Tooth Disease type 2 (CMT-2) or distal hereditary motor neuropathy (dHMN). Protein aggregation and axonal transport deficits have been implicated in the disease. In this study, we conducted analysis of bidirectional movements of mitochondria in primary motor neuron axons expressing wild type and mutant Hsp27. We found significantly slower retrograde transport of mitochondria in Ser135Phe, Pro39Leu and Arg140Gly mutant Hsp27 expressing motor neurons than in wild type Hsp27 neurons, although anterograde movement velocities remained normal. Retrograde transport of other important cargoes, such as the p75 neurotrophic factor receptor was minimally altered in mutant Hsp27 neurons, implicating that axonal transport deficits primarily affect mitochondria and the axonal transport machinery itself is less affected. Investigation of mitochondrial function revealed a decrease in mitochondrial membrane potential in mutant Hsp27 expressing motor axons, as well as a reduction in mitochondrial complex 1 activity, increased vulnerability of mitochondria to mitochondrial stressors, leading to elevated superoxide release and reduced mitochondrial glutathione (GSH) levels, although cytosolic GSH remained normal. This mitochondrial redox imbalance in mutant Hsp27 motor neurons is likely to cause low level of oxidative stress, which in turn will contribute to, and indeed may be the underlying cause of the deficits in mitochondrial axonal transport. Together, these findings suggest that the mitochondrial abnormalities in mutant Hsp27-induced neuropathies may be a primary cause of pathology, leading to further deficits in the mitochondrial axonal transport and onset of disease.
    MeSH term(s) Animals ; Axonal Transport/genetics ; Axonal Transport/physiology ; Axons/metabolism ; Cell Culture Techniques ; Charcot-Marie-Tooth Disease/genetics ; Charcot-Marie-Tooth Disease/metabolism ; HSP27 Heat-Shock Proteins/genetics ; HSP27 Heat-Shock Proteins/metabolism ; Heat-Shock Proteins/metabolism ; Mice ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Motor Neurons/metabolism ; Mutation ; Neoplasm Proteins/genetics
    Chemical Substances HSP27 Heat-Shock Proteins ; Heat-Shock Proteins ; Hspb2 protein, mouse ; Neoplasm Proteins
    Language English
    Publishing date 2017-06-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddx216
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  10. Article ; Online: Decay in survival motor neuron and plastin 3 levels during differentiation of iPSC-derived human motor neurons.

    Boza-Morán, María G / Martínez-Hernández, Rebeca / Bernal, Sara / Wanisch, Klaus / Also-Rallo, Eva / Le Heron, Anita / Alías, Laura / Denis, Cécile / Girard, Mathilde / Yee, Jiing-Kuan / Tizzano, Eduardo F / Yáñez-Muñoz, Rafael J

    Scientific reports

    2015  Volume 5, Page(s) 11696

    Abstract: Spinal muscular atrophy (SMA) is a neuromuscular disease caused by mutations in Survival Motor Neuron 1 (SMN1), leading to degeneration of alpha motor neurons (MNs) but also affecting other cell types. Induced pluripotent stem cell (iPSC)-derived human ... ...

    Abstract Spinal muscular atrophy (SMA) is a neuromuscular disease caused by mutations in Survival Motor Neuron 1 (SMN1), leading to degeneration of alpha motor neurons (MNs) but also affecting other cell types. Induced pluripotent stem cell (iPSC)-derived human MN models from severe SMA patients have shown relevant phenotypes. We have produced and fully characterized iPSCs from members of a discordant consanguineous family with chronic SMA. We differentiated the iPSC clones into ISL-1+/ChAT+ MNs and performed a comparative study during the differentiation process, observing significant differences in neurite length and number between family members. Analyses of samples from wild-type, severe SMA type I and the type IIIa/IV family showed a progressive decay in SMN protein levels during iPSC-MN differentiation, recapitulating previous observations in developmental studies. PLS3 underwent parallel reductions at both the transcriptional and translational levels. The underlying, progressive developmental decay in SMN and PLS3 levels may lead to the increased vulnerability of MNs in SMA disease. Measurements of SMN and PLS3 transcript and protein levels in iPSC-derived MNs show limited value as SMA biomarkers.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Cell Differentiation ; Cell Survival ; Clone Cells ; Coculture Techniques ; Female ; Humans ; Induced Pluripotent Stem Cells/cytology ; Male ; Membrane Glycoproteins/metabolism ; Mice ; Microfilament Proteins/metabolism ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Muscle Fibers, Skeletal/cytology ; Neurites/metabolism ; Pedigree ; Survival of Motor Neuron 1 Protein/metabolism
    Chemical Substances Biomarkers ; Membrane Glycoproteins ; Microfilament Proteins ; SMN1 protein, human ; Survival of Motor Neuron 1 Protein ; plastin
    Language English
    Publishing date 2015-06-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep11696
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