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  1. Article ; Online: Ivabradine acutely improves cardiac Ca handling and function in a rat model of Duchenne muscular dystrophy.

    Szabo, Petra Lujza / Marksteiner, Jessica / Ebner, Janine / Dostal, Christopher / Podesser, Bruno K / Sauer, Jakob / Kubista, Helmut / Todt, Hannes / Hackl, Benjamin / Koenig, Xaver / Kiss, Attila / Hilber, Karlheinz

    Physiological reports

    2023  Volume 11, Issue 7, Page(s) e15664

    Abstract: The muscular dystrophies caused by dystrophin deficiency, the so-called dystrophinopathies, are associated with impaired cardiac contractility and arrhythmias, which considerably contribute to disease morbidity and mortality. Impaired Ca handling in ... ...

    Abstract The muscular dystrophies caused by dystrophin deficiency, the so-called dystrophinopathies, are associated with impaired cardiac contractility and arrhythmias, which considerably contribute to disease morbidity and mortality. Impaired Ca handling in ventricular cardiomyocytes has been identified as a causative factor for complications in the dystrophic heart, and restoration of normal Ca handling in myocytes has emerged as a promising new therapeutic strategy. In the present study, we explored the hypothesis that ivabradine, a drug clinically approved for the treatment of heart failure and stable angina pectoris, improves Ca handling in dystrophic cardiomyocytes and thereby enhances contractile performance in the dystrophic heart. Therefore, ventricular cardiomyocytes were isolated from the hearts of adult dystrophin-deficient DMD
    MeSH term(s) Mice ; Rats ; Animals ; Dystrophin ; Muscular Dystrophy, Duchenne/complications ; Muscular Dystrophy, Duchenne/drug therapy ; Ivabradine/pharmacology ; Ivabradine/therapeutic use ; Mice, Inbred mdx ; Myocytes, Cardiac ; Disease Models, Animal
    Chemical Substances Dystrophin ; Ivabradine (3H48L0LPZQ)
    Language English
    Publishing date 2023-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15664
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Ubiquitin enzymes in the regulation of immune responses.

    Ebner, Petra / Versteeg, Gijs A / Ikeda, Fumiyo

    Critical reviews in biochemistry and molecular biology

    2017  Volume 52, Issue 4, Page(s) 425–460

    Abstract: Ubiquitination plays a central role in the regulation of various biological functions including immune responses. Ubiquitination is induced by a cascade of enzymatic reactions by E1 ubiquitin activating enzyme, E2 ubiquitin conjugating enzyme, and E3 ... ...

    Abstract Ubiquitination plays a central role in the regulation of various biological functions including immune responses. Ubiquitination is induced by a cascade of enzymatic reactions by E1 ubiquitin activating enzyme, E2 ubiquitin conjugating enzyme, and E3 ubiquitin ligase, and reversed by deubiquitinases. Depending on the enzymes, specific linkage types of ubiquitin chains are generated or hydrolyzed. Because different linkage types of ubiquitin chains control the fate of the substrate, understanding the regulatory mechanisms of ubiquitin enzymes is central. In this review, we highlight the most recent knowledge of ubiquitination in the immune signaling cascades including the T cell and B cell signaling cascades as well as the TNF signaling cascade regulated by various ubiquitin enzymes. Furthermore, we highlight the TRIM ubiquitin ligase family as one of the examples of critical E3 ubiquitin ligases in the regulation of immune responses.
    MeSH term(s) B-Lymphocytes/immunology ; Humans ; Signal Transduction ; T-Lymphocytes/immunology ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
    Chemical Substances Ubiquitin ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2017-05-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1000977-2
    ISSN 1549-7798 ; 1381-3455 ; 1040-9238
    ISSN (online) 1549-7798
    ISSN 1381-3455 ; 1040-9238
    DOI 10.1080/10409238.2017.1325829
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1024: Show issues Location:
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  3. Article ; Online: Reduced Na

    Ebner, Janine / Uhrin, Pavel / Szabo, Petra L / Kiss, Attila / Podesser, Bruno K / Todt, Hannes / Hilber, Karlheinz / Koenig, Xaver

    American journal of physiology. Heart and circulatory physiology

    2020  Volume 318, Issue 6, Page(s) H1436–H1440

    Abstract: Cardiac arrhythmias significantly contribute to mortality in Duchenne muscular dystrophy (DMD), a degenerative muscle disease triggered by mutations in the gene encoding for the intracellular protein dystrophin. A major source for the arrhythmias in ... ...

    Abstract Cardiac arrhythmias significantly contribute to mortality in Duchenne muscular dystrophy (DMD), a degenerative muscle disease triggered by mutations in the gene encoding for the intracellular protein dystrophin. A major source for the arrhythmias in patients with DMD is impaired ventricular impulse conduction, which predisposes for ventricular asynchrony, decreased cardiac output, and the development of reentrant mechanisms. The reason for ventricular conduction impairments and the associated arrhythmias in the dystrophic heart has remained unidentified. In the present study, we explored the hypothesis that dystrophin-deficient cardiac Purkinje fibers have reduced Na
    MeSH term(s) Action Potentials/physiology ; Animals ; Arrhythmias, Cardiac/complications ; Arrhythmias, Cardiac/metabolism ; Arrhythmias, Cardiac/physiopathology ; Cardiac Conduction System Disease/complications ; Cardiac Conduction System Disease/metabolism ; Cardiac Conduction System Disease/physiopathology ; Male ; Mice ; Mice, Inbred mdx ; Muscular Dystrophy, Duchenne/complications ; Muscular Dystrophy, Duchenne/metabolism ; Muscular Dystrophy, Duchenne/physiopathology ; Purkinje Fibers/metabolism ; Sodium/metabolism ; Sodium Channels/metabolism
    Chemical Substances Sodium Channels ; Sodium (9NEZ333N27)
    Language English
    Publishing date 2020-05-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00224.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Die Rolle der Frau im Wandel der Zeit

    Ebner, Petra

    Aktuelle Entwicklungen im österreichischen Gesundheits- und Pflegemanagement : Probleme - Analysen - Perspektiven , p. 241-260

    die Vereinbarung von Familie und Beruf von Frauen in Führungspositionen in der Krankenpflege

    2007  , Page(s) 241–260

    Author's details Petra Ebner
    Keywords Familie-Beruf ; Weibliche Führungskräfte ; Pflegeberufe ; Österreich
    Language German
    Publisher Facultas.wuv
    Publishing place Wien
    Document type Article
    ISBN 978-385-07680-3-0 ; 385-07680-3-1
    Database ECONomics Information System

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  5. Article ; Online: The IAP family member BRUCE regulates autophagosome–lysosome fusion

    Petra Ebner / Isabella Poetsch / Luiza Deszcz / Thomas Hoffmann / Johannes Zuber / Fumiyo Ikeda

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 15

    Abstract: The inhibitor of apoptosis (IAP) protein, BRUCE is known to ubiquitinate apoptosis regulators for proteasomal degradation. Here the authors show that BRUCE provides a bridge between LAMP2 on lysosomes and Atg8 family proteins on autophagosomes to support ...

    Abstract The inhibitor of apoptosis (IAP) protein, BRUCE is known to ubiquitinate apoptosis regulators for proteasomal degradation. Here the authors show that BRUCE provides a bridge between LAMP2 on lysosomes and Atg8 family proteins on autophagosomes to support autophagosome-lysosome fusion.
    Keywords Science ; Q
    Language English
    Publishing date 2018-02-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: The IAP family member BRUCE regulates autophagosome–lysosome fusion

    Petra Ebner / Isabella Poetsch / Luiza Deszcz / Thomas Hoffmann / Johannes Zuber / Fumiyo Ikeda

    Nature Communications, Vol 9, Iss 1, Pp 1-

    2018  Volume 15

    Abstract: The inhibitor of apoptosis (IAP) protein, BRUCE is known to ubiquitinate apoptosis regulators for proteasomal degradation. Here the authors show that BRUCE provides a bridge between LAMP2 on lysosomes and Atg8 family proteins on autophagosomes to support ...

    Abstract The inhibitor of apoptosis (IAP) protein, BRUCE is known to ubiquitinate apoptosis regulators for proteasomal degradation. Here the authors show that BRUCE provides a bridge between LAMP2 on lysosomes and Atg8 family proteins on autophagosomes to support autophagosome-lysosome fusion.
    Keywords Science ; Q
    Language English
    Publishing date 2018-02-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: The IAP family member BRUCE regulates autophagosome-lysosome fusion.

    Ebner, Petra / Poetsch, Isabella / Deszcz, Luiza / Hoffmann, Thomas / Zuber, Johannes / Ikeda, Fumiyo

    Nature communications

    2018  Volume 9, Issue 1, Page(s) 599

    Abstract: Autophagy has an important role in cellular homeostasis by degrading and recycling cytotoxic components. Ubiquitination is known to target cargoes for autophagy; however, key components of this pathway remain elusive. Here we performed an RNAi screen to ... ...

    Abstract Autophagy has an important role in cellular homeostasis by degrading and recycling cytotoxic components. Ubiquitination is known to target cargoes for autophagy; however, key components of this pathway remain elusive. Here we performed an RNAi screen to uncover ubiquitin modifiers that are required for starvation-induced macroautophagy in mammalian cells. Our screen uncovered BRUCE/Apollon/Birc6, an IAP protein, as a new autophagy regulator. Depletion of BRUCE leads to defective fusion of autophagosomes and lysosomes. Mechanistically, BRUCE selectively interacts with two ATG8 members GABARAP and GABARAPL1, as well as with Syntaxin 17, which are all critical regulators of autophagosome-lysosome fusion. In addition, BRUCE colocalizes with LAMP2. Interestingly, a non-catalytic N-terminal BRUCE fragment that is sufficient to bind GABARAP/GABARAPL1 and Syntaxin 17, and to colocalize with LAMP2, rescues autolysosome formation in Bruce
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apoptosis/genetics ; Apoptosis Regulatory Proteins ; Autophagosomes/metabolism ; Autophagy/genetics ; CRISPR-Cas Systems ; Cell Line ; Cells, Cultured ; HEK293 Cells ; Humans ; Inhibitor of Apoptosis Proteins/genetics ; Inhibitor of Apoptosis Proteins/metabolism ; Lysosomes/genetics ; Lysosomes/metabolism ; Membrane Fusion ; Mice, Knockout ; Microscopy, Fluorescence ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Protein Binding ; RNA Interference
    Chemical Substances Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; GABARAP protein, human ; GABARAPL1 protein, human ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins
    Language English
    Publishing date 2018-02-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-018-02823-x
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  8. Article ; Online: A semisynthetic glycoconjugate provides expanded cross-serotype protection against Streptococcus pneumoniae.

    Kaplonek, Paulina / Yao, Ling / Reppe, Katrin / Voß, Franziska / Kohler, Thomas / Ebner, Friederike / Schäfer, Alexander / Blohm, Ulrike / Priegue, Patricia / Bräutigam, Maria / Pereira, Claney L / Parameswarappa, Sharavathi G / Emmadi, Madhu / Ménová, Petra / Witzenrath, Martin / Hammerschmidt, Sven / Hartmann, Susanne / Sander, Leif E / Seeberger, Peter H

    Vaccine

    2022  Volume 40, Issue 7, Page(s) 1038–1046

    Abstract: Streptococcus pneumoniae (S. pneumoniae)infections are the leading cause of child mortality globally. Currentvaccines fail to induceaprotective immune response towards a conserved part of the pathogen,resulting in newserotypescausing disease. Therefore, ... ...

    Abstract Streptococcus pneumoniae (S. pneumoniae)infections are the leading cause of child mortality globally. Currentvaccines fail to induceaprotective immune response towards a conserved part of the pathogen,resulting in newserotypescausing disease. Therefore, new vaccinestrategies are urgently needed.Described is atwo-pronged approach combiningS. pneumoniaeproteins, pneumolysin (Ply) and pneumococcal surface protein A (PspA),with aprecisely defined synthetic oligosaccharide,wherebythe carrier protein actsas a serotype-independent antigen to provideadditional protection. Proof of concept in mice and swine modelsrevealed thatthe conjugatesinhibited colonization of the nasopharynx, decreased the bacterial load and reduced disease severity in the bacteria challenge model. Immunization of piglets provided the first evidence for the immunogenicity and protective potential of synthetic glycoconjugate vaccine in a large animal model.Acombination of synthetic oligosaccharides with proteins from the target pathogen opens the path to create broadly cross-protective ("universal") pneumococcal vaccines.
    MeSH term(s) Animals ; Antibodies, Bacterial ; Bacterial Proteins ; Glycoconjugates ; Mice ; Pneumococcal Infections ; Pneumococcal Vaccines ; Serogroup ; Streptococcus pneumoniae ; Swine
    Chemical Substances Antibodies, Bacterial ; Bacterial Proteins ; Glycoconjugates ; Pneumococcal Vaccines
    Language English
    Publishing date 2022-01-13
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605674-x
    ISSN 1873-2518 ; 0264-410X
    ISSN (online) 1873-2518
    ISSN 0264-410X
    DOI 10.1016/j.vaccine.2021.12.068
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1930: Show issues Location:
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  9. Article ; Online: Cardiovascular phenotype of the

    Szabó, Petra Lujza / Ebner, Janine / Koenig, Xaver / Hamza, Ouafa / Watzinger, Simon / Trojanek, Sandra / Abraham, Dietmar / Todt, Hannes / Kubista, Helmut / Schicker, Klaus / Remy, Séverine / Anegon, Ignacio / Kiss, Attila / Podesser, Bruno K / Hilber, Karlheinz

    Disease models & mechanisms

    2021  Volume 14, Issue 2

    Abstract: Besides skeletal muscle abnormalities, Duchenne muscular dystrophy (DMD) patients present with dilated cardiomyopathy development, which considerably contributes to morbidity and mortality. Because the mechanisms responsible for the cardiac complications ...

    Abstract Besides skeletal muscle abnormalities, Duchenne muscular dystrophy (DMD) patients present with dilated cardiomyopathy development, which considerably contributes to morbidity and mortality. Because the mechanisms responsible for the cardiac complications in the context of DMD are largely unknown, evidence-based therapy approaches are still lacking. This has increased the need for basic research efforts into animal models for DMD. Here, we characterized in detail the cardiovascular abnormalities of
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channels, L-Type/metabolism ; Cardiomyopathies/pathology ; Cardiomyopathy, Dilated/complications ; Cardiovascular System ; Disease Models, Animal ; Dystrophin/genetics ; Dystrophin/metabolism ; Endothelium, Vascular/pathology ; Fibrosis/pathology ; Heart Ventricles/physiopathology ; Hemodynamics ; Homeostasis ; Humans ; Inflammation ; Kidney/metabolism ; Lung/metabolism ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Duchenne/genetics ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Oxidative Stress ; Peptidyl-Dipeptidase A ; Phenotype ; Rats ; Stress, Mechanical
    Chemical Substances CACNA1C protein, human ; Calcium Channels, L-Type ; DMD protein, human ; Dmd protein, rat ; Dystrophin ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-02-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.047704
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The domestic pig as human-relevant large animal model to study adaptive antifungal immune responses against airborne Aspergillus fumigatus.

    Schmidt, Stefanie / Ebner, Friederike / Rosen, Kerstin / Kniemeyer, Olaf / Brakhage, Axel A / Löffler, Jürgen / Seif, Michelle / Springer, Jan / Schlosser, Josephine / Scharek-Tedin, Lydia / Scheffold, Alexander / Bacher, Petra / Kühl, Anja A / Rösler, Uwe / Hartmann, Susanne

    European journal of immunology

    2020  Volume 50, Issue 11, Page(s) 1712–1728

    Abstract: Pulmonary mucosal immune response is critical for preventing opportunistic Aspergillus fumigatus infections. Although fungus-specific ... ...

    Abstract Pulmonary mucosal immune response is critical for preventing opportunistic Aspergillus fumigatus infections. Although fungus-specific CD4
    MeSH term(s) Animals ; Antifungal Agents/immunology ; Aspergillus/immunology ; Aspergillus fumigatus/immunology ; Disease Models, Animal ; Host-Pathogen Interactions/immunology ; Humans ; Lung/immunology ; Spores, Fungal/immunology ; Sus scrofa/immunology ; Swine ; Th1 Cells/immunology
    Chemical Substances Antifungal Agents
    Language English
    Publishing date 2020-07-13
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201948524
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    Zs.MG 85: Show issues

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