Now showing 1 - 10 of 99
  • 2011Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","521"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","528"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","Aims The calcineurin and nuclear factor of activated T cells (NFAT) pathway can mediate pro-hypertrophic signalling in the heart. Recently, it has been shown that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) phosphorylates NFAT, which limits calcineurin/NFAT signal transduction in T cells and hypertrophy in cultured cardiomyocytes. The hypothesis tested in this study was that DYRK1A prevents calcineurin/NFAT-mediated cardiac hypertrophy in vivo. Methods and results In cultured rat cardiomyocytes, adenovirus-mediated overexpression of DYRK1A antagonized calcineurin-mediated nuclear NFAT translocation and the phenylephrine-induced hypertrophic growth response. To test the ability of DYRK1A to reduce hypertrophic cardiac growth in vivo, we created tetracycline-repressible Dyrk1a transgenic mice to avoid the cardiac developmental defects associated with embryonic DYRK1A expression. However, in the mouse model, histological determination of myocyte diameter, heart weight/body weight ratio, and echocardiographic measurements revealed that myocardial expression of DYRK1A failed to reduce hypertrophy induced via aortic banding or co-expression of calcineurin. This discrepancy is explained, at least in part, by insufficient long-term inhibition of NFAT and the activation of DYRK1A-resistant maladaptive genes in vivo. Conclusion Isolated augmentation of DYRK1A can be compensated for in vivo, and this may significantly limit anti-hypertrophic interventions aimed at enhancing DYRK1A activity."],["dc.identifier.doi","10.1093/cvr/cvr023"],["dc.identifier.gro","3142722"],["dc.identifier.isi","000290820200018"],["dc.identifier.pmid","21273244"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/157"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2005Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Higuchi, Yoshiharu"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Wand, Saskia"],["dc.contributor.author","Kramps, P."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T10:56:04Z"],["dc.date.available","2018-11-07T10:56:04Z"],["dc.date.issued","2005"],["dc.format.extent","99"],["dc.identifier.isi","000233987100392"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49927"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","27th Congress of the European-Society-of-Cardiology"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Adenoviral expression of short interfering RNA effectively silences gene expression in adult rabbit cardiac myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2009Conference Abstract
    [["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T11:24:12Z"],["dc.date.available","2018-11-07T11:24:12Z"],["dc.date.issued","2009"],["dc.format.extent","E18"],["dc.identifier.isi","000270150800052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56350"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","Basic Cardiovascular Sciences Conference 2009"],["dc.relation.eventlocation","Lake Las Vegas, Henderson, NV"],["dc.relation.issn","0009-7330"],["dc.title","Dual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A (DYRK1A) Strongly Antagonizes Calcineurin/NFAT Signaling but Can Be Prohypertrophic on Overexpression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2003Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","996"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Ohler, A."],["dc.contributor.author","Embry, S. L."],["dc.contributor.author","Muller, F"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Kogler, H."],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2021-06-01T10:50:03Z"],["dc.date.available","2021-06-01T10:50:03Z"],["dc.date.issued","2003"],["dc.description.abstract","Objectives: The functional consequences of Na+/Ca2+ exchanger (NCX) overexpression in heart failure have been controversially discussed. NCX function strongly depends on intracellular sodium which has been shown to be increased in heart failure. Methods and results: We investigated the Na+/K+-ATPase (NKA) inhibitor ouabain (0.5-16 mumol/l) in electrically stimulated, isotonically contracting adult rabbit cardiocytes overexpressing NCX after adenoviral gene transfer (Ad-NCX-GFP, 48 h culture time). Myocytes transfected with adenovirus encoding for green fluorescent protein (Ad-GFP) served as a control. Contractions were analyzed by video-edge detection. In the Ad-NCX-GFP group, the maximum inotropic response was significantly reduced by 50.7% (P < 0.05). This was a result of an enhanced susceptibility to contracture after exposure to the drug (median concentration (25-75%): 4 (4-8) vs. 8 (6-16) mumol/l, P < 0.05). When analyzing relaxation before contracture, the maximum relaxation velocity was reduced (0.15 +/- 0.04 vs. 0.27 +/- 0.04 mum/s, P < 0.05) and the time from peak shortening to 90% of relaxation was increased (298 +/- 39 vs. 185 +/- 15 ms, P < 0.05). No differences in systolic and diastolic parameters were observed with the Na+ channel modulator BDF9198 (1 mumol/l). Conclusions: Inhibition of NKA by ouabain induces a combined diastolic and systolic dysfunction in NCX overexpressing rabbit myocytes. This may be the consequence of cytoplasmic Ca2+ overload due to inhibition of forward mode or induction of reverse mode Na+/Ca2+ exchange. In end-stage failing human myocardium and during digitalis treatment this mechanism may be of major importance. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0008-6363(02)00829-5"],["dc.identifier.gro","3144121"],["dc.identifier.isi","000181975100014"],["dc.identifier.pmid","12650877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86511"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","The functional effect of adenoviral Na+/Ca2+ exchanger overexpression in rabbit myocytes depends on the activity of the Na+/K+-ATPase"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, T. M."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T11:11:19Z"],["dc.date.available","2018-11-07T11:11:19Z"],["dc.date.issued","2008"],["dc.format.extent","712"],["dc.identifier.isi","000208702503546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53407"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Dual-specificity tyrosine phosphorylation-regulated kinase 1A is a NFAT kinase mediating negative feedback on Calcineurin/NFAT signaling in cardiac myocytes"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schuster, Manfred"],["dc.contributor.author","Loibner, Hans"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kuba, Keiji"],["dc.contributor.author","Imai, Yumiko"],["dc.contributor.author","Penninger, Josef"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T11:09:55Z"],["dc.date.available","2018-11-07T11:09:55Z"],["dc.date.issued","2008"],["dc.format.extent","S947"],["dc.identifier.isi","000262104503504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53105"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Angiotensin-Converting-Enzyme 2 (rhACE2) Potently Attenuates the Negative Hemodynamic Effects of Angiotensin II (ATII) and Improves Post-Myocardial Infarction (MI) Remodeling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2004Conference Abstract
    [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Miller, S."],["dc.contributor.author","Reynolds, D."],["dc.contributor.author","Currie, S."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Smith, G."],["dc.date.accessioned","2018-11-07T10:52:09Z"],["dc.date.available","2018-11-07T10:52:09Z"],["dc.date.issued","2004"],["dc.format.extent","49A"],["dc.identifier.isi","000187971200250"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49051"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biophysical Society"],["dc.publisher.place","Bethesda"],["dc.relation.conference","48th Annual Meeting of the Biophysical Society"],["dc.relation.eventlocation","Baltimore, MD"],["dc.relation.issn","0006-3495"],["dc.title","Calsequestrin: A modulator of excitation-contraction coupling in rabbit cardiomyocytes."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2008Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Maier, Lars. S."],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.date.accessioned","2018-11-07T11:11:18Z"],["dc.date.available","2018-11-07T11:11:18Z"],["dc.date.issued","2008"],["dc.format.extent","265"],["dc.identifier.isi","000208702501245"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53401"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Large volume, ice-cold intravenous fluid for therapeutic hypothermia does not compromise the respiratory situation in patients after cardiac arrest"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","744"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Klingebiel, Theda-Maria"],["dc.contributor.author","Grau, Simon Philipp"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","HasenfuĂź, Gerd"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T08:52:46Z"],["dc.date.available","2018-11-07T08:52:46Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1093/cvr/cvr193"],["dc.identifier.isi","000294069300024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22252"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0008-6363"],["dc.title","Letter concerning: 'Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo': reply"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]
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  • 2004Conference Abstract
    [["dc.bibliographiccitation.firstpage","178"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","179"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Kohlhaas, M."],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Zhang, T."],["dc.contributor.author","Zibrova, D."],["dc.contributor.author","Dybkova, Nataliya"],["dc.contributor.author","Brown, Joan Heller"],["dc.contributor.author","Bers, Donald M."],["dc.contributor.author","Maier, Lars. S."],["dc.date.accessioned","2018-11-07T10:46:37Z"],["dc.date.available","2018-11-07T10:46:37Z"],["dc.date.issued","2004"],["dc.identifier.isi","000224056500714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47789"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.publisher.place","London"],["dc.relation.conference","ESC Congress 2004"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0195-668X"],["dc.title","Intracellular calcium handling in isolated rabbit cardiac myocytes overexpressing cytoplasmic vs. nuclear CaMKIIdelta isoform"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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