El-Armouche, Ali

[["dc.bibliographiccitation.firstpage","165"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","175"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Wittig, Karola"],["dc.contributor.author","Vogt, Andreas"],["dc.contributor.author","Wuertz, Christina M."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Wieland, Thomas"],["dc.date.accessioned","2018-11-07T09:07:59Z"],["dc.date.available","2018-11-07T09:07:59Z"],["dc.date.issued","2012"],["dc.description.abstract","Activation of alpha(1)-adrenoceptors (alpha(1)-AR) by high catecholamine levels, e.g. in heart failure, is thought to be a driving force of cardiac hypertrophy. In this context several downstream mediators and cascades have been identified to potentially play a role in cardiomyocyte hypertrophy. One of these proteins is the monomeric G protein Rac1. However, until now it is unclear how this essential G protein is activated by alpha(1)-AR agonists and what are the downstream targets inducing cellular growth. By using protein-based as well as pharmacological inhibitors and the shRNA technique, we demonstrate that in neonatal rat cardiomyocytes (NRCM) Rac1 is activated via a cascade involving the alpha(1A)-AR subtype, G(i)beta gamma, the phosphoinositide-3'-kinase and the guanine nucleotide exchange factor Tiam1. We further demonstrate that this signaling induces an increase in protein synthesis, cell size and atrial natriuretic peptide expression. We identified the p21-activated kinase 2 (PAK2) as a downstream effector of Rac1 and were able to link this cascade to the activation of the pro-hypertrophic kinases ERK1/2 and p90RSK. Our data thus reveal a prominent role of the alpha(1A)-AR/G(i)beta gamma/Tiam1-mediated activation of Rac1 and its effector PAK2 in the induction of hypertrophy in NRCM. (C) 2012 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.yjmcc.2012.04.015"],["dc.identifier.isi","000306451600003"],["dc.identifier.pmid","22564263"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25922"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.title","A novel player in cellular hypertrophy: G(i)beta gamma/PI3K-dependent activation of the RacGEF TIAM-1 is required for alpha(1)-adrenoceptor induced hypertrophy in neonatal rat cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","599a"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Lindner, Marta"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Riedel, Merle"],["dc.contributor.author","Lämmle, Simon"],["dc.contributor.author","Mason, Fleur"],["dc.contributor.author","Meinecke, Simon"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Karam, Sarah"],["dc.contributor.author","Lechene, Patrick"],["dc.contributor.author","Leroy, Jerome"],["dc.contributor.author","Vandecasteele, Gregoire"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.date.accessioned","2020-12-10T14:22:42Z"],["dc.date.available","2020-12-10T14:22:42Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.bpj.2015.11.3199"],["dc.identifier.issn","0006-3495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71701"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cardiac-Specific Overexpression of Phosphodiesterase 2 (PDE2) in Mouse is Cardioprotective"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Gene Therapy"],["dc.bibliographiccitation.lastpage","19"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Schwab, D M"],["dc.contributor.author","Tilemann, L"],["dc.contributor.author","Bauer, R"],["dc.contributor.author","Heckmann, M"],["dc.contributor.author","Jungmann, A"],["dc.contributor.author","Wagner, M"],["dc.contributor.author","Burgis, J"],["dc.contributor.author","Vettel, C"],["dc.contributor.author","Katus, H A"],["dc.contributor.author","El-Armouche, A"],["dc.contributor.author","Müller, O J"],["dc.date.accessioned","2020-12-10T18:09:27Z"],["dc.date.available","2020-12-10T18:09:27Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/gt.2017.97"],["dc.identifier.eissn","1476-5462"],["dc.identifier.issn","0969-7128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73660"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","AAV-9 mediated phosphatase-1 inhibitor-1 overexpression improves cardiac contractility in unchallenged mice but is deleterious in pressure-overload"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1596"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Journal of the American College of Cardiology"],["dc.bibliographiccitation.lastpage","1606"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Emons, Julius"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Wittköpper, Katrin"],["dc.contributor.author","Seppelt, Danilo"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Lutz, Susanne"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Lechêne, Patrick"],["dc.contributor.author","Leroy, Jérôme"],["dc.contributor.author","Lefebvre, Florence"],["dc.contributor.author","Varin, Audrey"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Nattel, Stanley"],["dc.contributor.author","Dobrev, Dobromir"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Vandecasteele, Grégoire"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2019-01-14T16:02:22Z"],["dc.date.available","2019-01-14T16:02:22Z"],["dc.date.issued","2013"],["dc.description.abstract","Objectives This study investigated whether myocardial phosphodiesterase-2 (PDE2) is altered in heart failure (HF) and determined PDE2-mediated effects on beta-adrenergic receptor (β-AR) signaling in healthy and diseased cardiomyocytes. Background Diminished cyclic adenosine monophosphate (cAMP) and augmented cyclic guanosine monophosphate (cGMP) signaling is characteristic for failing hearts. Among the PDE superfamily, PDE2 has the unique property of being able to be stimulated by cGMP, thus leading to a remarkable increase in cAMP hydrolysis mediating a negative cross talk between cGMP and cAMP signaling. However, the role of PDE2 in HF is poorly understood. Methods Immunoblotting, radioenzymatic- and fluorescence resonance energy transfer–based assays, video edge detection, epifluorescence microscopy, and L-type Ca2+ current measurements were performed in myocardial tissues and/or isolated cardiomyocytes from human and/or experimental HF, respectively. Results Myocardial PDE2 expression and activity were ∼2-fold higher in advanced human HF. Chronic β-AR stimulation via catecholamine infusions in rats enhanced PDE2 expression ∼2-fold and cAMP hydrolytic activity ∼4-fold, which correlated with blunted cardiac β-AR responsiveness. In diseased cardiomyocytes, higher PDE2 activity could be further enhanced by stimulation of cGMP synthesis via nitric oxide donors, whereas specific PDE2 inhibition partially restored β-AR responsiveness. Accordingly, PDE2 overexpression in healthy cardiomyocytes reduced the rise in cAMP levels and L-type Ca2+ current amplitude, and abolished the inotropic effect following acute β-AR stimulation, without affecting basal contractility. Importantly, PDE2-overexpressing cardiomyocytes showed marked protection from norepinephrine-induced hypertrophic responses. Conclusions PDE2 is markedly up-regulated in failing hearts and desensitizes against acute β-AR stimulation. This may constitute an important defense mechanism during cardiac stress, for example, by antagonizing excessive β-AR drive. Thus, activating myocardial PDE2 may represent a novel intracellular antiadrenergic therapeutic strategy in HF."],["dc.identifier.doi","10.1016/j.jacc.2013.05.057"],["dc.identifier.gro","3142269"],["dc.identifier.isi","000325937400010"],["dc.identifier.pmid","23810893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57317"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/37"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A01: cAMP- und cGMP- Mikrodomänen bei Herzhypertrophie und Insuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.eissn","1558-3597"],["dc.relation.issn","1558-3597"],["dc.relation.issn","0735-1097"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Phosphodiesterase-2 Is Up-Regulated in Human Failing Hearts and Blunts β-Adrenergic Responses in Cardiomyocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","819"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Heart"],["dc.bibliographiccitation.lastpage","820"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2019-02-05T10:29:11Z"],["dc.date.available","2019-02-05T10:29:11Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1136/heartjnl-2014-305503"],["dc.identifier.pmid","24667282"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57520"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/9"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation.issn","1468-201X"],["dc.relation.workinggroup","RG El-Armouche"],["dc.title","The Janus face of BNP therapy in chronic heart failure: beneficial effects unmasked by β blockers?"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","editorial_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e003840"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Circulation: Heart Failure"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Neef, Stefan"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Lämmle, Simon"],["dc.contributor.author","Beushausen, Christina"],["dc.contributor.author","Zelarayan, Laura C."],["dc.contributor.author","Katz, Sylvia"],["dc.contributor.author","von der Lieth, Albert"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Weber, Silvio"],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Backs, Johannes"],["dc.contributor.author","Brown, Joan H."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2020-12-10T18:37:57Z"],["dc.date.available","2020-12-10T18:37:57Z"],["dc.date.issued","2017"],["dc.description.abstract","Background— Considerable evidence suggests that calcium/calmodulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology of heart failure (HF), a condition characterized by excessive β-adrenoceptor (β-AR) stimulation. Recent studies indicate a significant cross talk between β-AR signaling and CaMKII activation presenting CaMKII as a possible downstream mediator of detrimental β-AR signaling in HF. In this study, we investigated the effect of chronic β-AR blocker treatment on CaMKII activity in human and experimental HF. Methods and Results— Immunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF subjects undergoing cardiac surgery (n=12) treated with β-AR blockers revealed no difference in CaMKII activity when compared with non–β-AR blocker–treated patients. CaMKII activity was judged by analysis of CaMKII expression, autophosphorylation, and oxidation and by investigating the phosphorylation status of CaMKII downstream targets. To further evaluate these findings, CaMKIIδC transgenic mice were treated with the β1-AR blocker metoprolol (270 mg/kg d). Metoprolol significantly reduced transgene-associated mortality (n≥29; P<0.001), attenuated the development of cardiac hypertrophy (−14±6% heart weight/tibia length; P<0.05), and strongly reduced ventricular arrhythmias (−70±22% premature ventricular contractions; P<0.05). On a molecular level, metoprolol expectedly decreased protein kinase A–dependent phospholamban and ryanodine receptor 2 phosphorylation (−42±9% for P-phospholamban-S16 and −22±7% for P-ryanodine receptor 2-S2808; P<0.05). However, this was paralled neither by a reduction in CaMKII autophosphorylation, oxidation, and substrate binding nor a change in the phosphorylation of CaMKII downstream target proteins (n≥11). The lack of CaMKII modulation by β-AR blocker treatment was confirmed in healthy wild-type mice receiving metoprolol. Conclusions— Chronic β-AR blocker therapy in patients and in a mouse model of CaMKII-induced HF is not associated with a change in CaMKII activity. Thus, our data suggest that the molecular effects of β-AR blockers are not based on a modulation of CaMKII. Directly targeting CaMKII may, therefore, further improve HF therapy in addition to β-AR blockade."],["dc.identifier.doi","10.1161/CIRCHEARTFAILURE.117.003840"],["dc.identifier.pmid","28487342"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77149"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/171"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation.issn","1941-3289"],["dc.relation.issn","1941-3297"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic β-Adrenoceptor Blockade in Experimental and Human Heart Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S67"],["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.lastpage","S68"],["dc.bibliographiccitation.volume","387"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T09:44:49Z"],["dc.date.available","2018-11-07T09:44:49Z"],["dc.date.issued","2014"],["dc.identifier.isi","000359538500273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34478"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","80th Annual Meeting of the Deutsche-Gesellschaft-fur-Experimentelle-und-Klinische-Pharmakologie-und Toxikologie-e-V"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Development of molecular imaging tools to investigate protein phosphatase type-1 and type-2A localisation and dynamics in living cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1004"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","1016"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Swain, Lija"],["dc.contributor.author","Kesemeyer, Andrea"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Zieseniss, Anke"],["dc.contributor.author","Güntsch, Annemarie"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Becker, Andreas"],["dc.contributor.author","Nanadikar, Maithily S."],["dc.contributor.author","Morgan, Bruce"],["dc.contributor.author","Dennerlein, Sven"],["dc.contributor.author","Shah, Ajay M."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Katschinski, Dörthe M."],["dc.date.accessioned","2020-12-10T18:37:59Z"],["dc.date.available","2020-12-10T18:37:59Z"],["dc.date.issued","2016"],["dc.description.abstract","Rationale: Changes in redox potentials of cardiac myocytes are linked to several cardiovascular diseases. Redox alterations are currently mostly described qualitatively using chemical sensors, which however do not allow quantifying redox potentials, lack specificity, and the possibility to analyze subcellular domains. Recent advances to quantitatively describe defined redox changes include the application of genetically encoded redox biosensors. Objective: Establishment of mouse models, which allow the quantification of the glutathione redox potential (E-GSH) in the cytoplasm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts based on the use of the redox-sensitive green fluorescent protein 2, coupled to the glutaredoxin 1 (Grx1-roGFP2). Methods and Results: We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 targeted either to the mitochondrial matrix or to the cytoplasm. The response of the roGFP2 toward H2O2, diamide, and dithiothreitol was titrated and used to determine the E-GSH in isolated cardiac myocytes and in Langendorff-perfused hearts. Distinct E-GSH were observed in the cytoplasm and the mitochondrial matrix. Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or exposure to hypoxia/reoxygenation additionally underscored that these compartments responded independently. A compartment-specific response was also observed 3 to 14 days after myocardial infarction. Conclusions: We introduce redox biosensor mice as a new tool, which allows quantification of defined alterations of E-GSH in the cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer questions in basic and translational cardiovascular research."],["dc.identifier.doi","10.1161/CIRCRESAHA.116.309551"],["dc.identifier.eissn","1524-4571"],["dc.identifier.isi","000386313900013"],["dc.identifier.issn","0009-7330"],["dc.identifier.pmid","27553648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77158"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1524-4571"],["dc.relation.issn","0009-7330"],["dc.title","Redox Imaging Using Cardiac Myocyte-Specific Transgenic Biosensor Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","387"],["dc.contributor.author","Saadatmand, Ali Reza"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Meyer-Roxlau, Stefanie"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Lehmann, Lorenz H."],["dc.contributor.author","Backs, Johannes"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2018-11-07T09:44:50Z"],["dc.date.available","2018-11-07T09:44:50Z"],["dc.date.issued","2014"],["dc.format.extent","S80"],["dc.identifier.isi","000359538500325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34485"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","80th Annual Meeting of the Deutsche-Gesellschaft-fur-Experimentelle-und-Klinische-Pharmakologie-und Toxikologie-e-V"],["dc.relation.eventlocation","Hannover, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","PKA and CaMKII- mediated phosphorylation of Histone H3S28 during pathological b-adrenergic stimulation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","120"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","132"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Vettel, Christiane"],["dc.contributor.author","Lindner, Marta"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Lorenz, Kristina"],["dc.contributor.author","Schanbacher, Constanze"],["dc.contributor.author","Riedel, Merle"],["dc.contributor.author","Lämmle, Simon"],["dc.contributor.author","Meinecke, Simone"],["dc.contributor.author","Mason, Fleur E."],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Geerts, Andreas"],["dc.contributor.author","Hoffmann, Michael"],["dc.contributor.author","Wunder, Frank"],["dc.contributor.author","Brunner, Fabian J."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Mehel, Hind"],["dc.contributor.author","Karam, Sarah"],["dc.contributor.author","Lechêne, Patrick"],["dc.contributor.author","Leroy, Jérôme"],["dc.contributor.author","Vandecasteele, Grégoire"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Fischmeister, Rodolphe"],["dc.contributor.author","El-Armouche, Ali"],["dc.date.accessioned","2020-12-10T18:37:59Z"],["dc.date.available","2020-12-10T18:37:59Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1161/CIRCRESAHA.116.310069"],["dc.identifier.pmid","27799254"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77159"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/309"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.title","Phosphodiesterase 2 Protects Against Catecholamine-Induced Arrhythmia and Preserves Contractile Function After Myocardial Infarction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]