Wagner, Eva

[["dc.bibliographiccitation.firstpage","S123.2"],["dc.bibliographiccitation.issue","suppl 1"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","S123"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Hebisch, Elke"],["dc.contributor.author","Steinbrecher, Julia H."],["dc.contributor.author","Westphal, Volker"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Hell, Stefan"],["dc.contributor.author","Lehnart, Stephan E."],["dc.date.accessioned","2017-09-07T11:53:09Z"],["dc.date.available","2017-09-07T11:53:09Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1093/cvr/cvu098.101"],["dc.identifier.gro","3145042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2734"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Oxford University Press (OUP)"],["dc.relation.issn","0008-6363"],["dc.title","P677Superresolution microscopy reveals proliferative T-Tubule remodeling as general disease mechanism in early stages of heart failure development"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Rudolph, Franziska"],["dc.contributor.author","Fink, Claudia"],["dc.contributor.author","Hüttemeister, Judith"],["dc.contributor.author","Kirchner, Marieluise"],["dc.contributor.author","Radke, Michael H."],["dc.contributor.author","Lopez Carballo, Jacobo"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Lehnart, Stephan Elmar"],["dc.contributor.author","Mertins, Philipp"],["dc.contributor.author","Gotthardt, Michael"],["dc.date.accessioned","2021-04-14T08:25:49Z"],["dc.date.available","2021-04-14T08:25:49Z"],["dc.date.issued","2020"],["dc.description.abstract","Proximity proteomics has greatly advanced the analysis of native protein complexes and subcellular structures in culture, but has not been amenable to study development and disease in vivo. Here, we have generated a knock-in mouse with the biotin ligase (BioID) inserted at titin’s Z-disc region to identify protein networks that connect the sarcomere to signal transduction and metabolism. Our census of the sarcomeric proteome from neonatal to adult heart and quadriceps reveals how perinatal signaling, protein homeostasis and the shift to adult energy metabolism shape the properties of striated muscle cells. Mapping biotinylation sites to sarcomere structures refines our understanding of myofilament dynamics and supports the hypothesis that myosin filaments penetrate Z-discs to dampen contraction. Extending this proof of concept study to BioID fusion proteins generated with Crispr/CAS9 in animal models recapitulating human pathology will facilitate the future analysis of molecular machines and signaling hubs in physiological, pharmacological, and disease context."],["dc.identifier.doi","10.1038/s41467-020-16929-8"],["dc.identifier.pmid","32561764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81738"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/358"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S02: Hochauflösende Fluoreszenzmikroskopie und integrative Datenanalyse"],["dc.relation.eissn","2041-1723"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.rights","CC BY 4.0"],["dc.title","Deconstructing sarcomeric structure–function relations in titin-BioID knock-in mice"],["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","402"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","414"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Lauterbach, Marcel A."],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Westphal, Volker"],["dc.contributor.author","Williams, George S. B."],["dc.contributor.author","Steinbrecher, Julia H."],["dc.contributor.author","Streich, Jan-Hendrik"],["dc.contributor.author","Korff, Brigitte"],["dc.contributor.author","Tuan, Hoang-Trong M."],["dc.contributor.author","Hagen, Brian"],["dc.contributor.author","Luther, Stefan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Parlitz, Ulrich"],["dc.contributor.author","Jafri, M. Saleet"],["dc.contributor.author","Hell, Stefan"],["dc.contributor.author","Lederer, W. Jonathan"],["dc.contributor.author","Lehnart, Stephan E."],["dc.date.accessioned","2017-09-07T11:48:29Z"],["dc.date.available","2017-09-07T11:48:29Z"],["dc.date.issued","2012"],["dc.description.abstract","Rationale: Transverse tubules (TTs) couple electric surface signals to remote intracellular Ca2+ release units (CRUs). Diffraction-limited imaging studies have proposed loss of TT components as disease mechanism in heart failure (HF). Objectives: Objectives were to develop quantitative super-resolution strategies for live-cell imaging of TT membranes in intact cardiomyocytes and to show that TT structures are progressively remodeled during HF development, causing early CRU dysfunction. Methods and Results: Using stimulated emission depletion (STED) microscopy, we characterized individual TTs with nanometric resolution as direct readout of local membrane morphology 4 and 8 weeks after myocardial infarction (4pMI and 8pMI). Both individual and network TT properties were investigated by quantitative image analysis. The mean area of TT cross sections increased progressively from 4pMI to 8pMI. Unexpectedly, intact TT networks showed differential changes. Longitudinal and oblique TTs were significantly increased at 4pMI, whereas transversal components appeared decreased. Expression of TT-associated proteins junctophilin-2 and caveolin-3 was significantly changed, correlating with network component remodeling. Computational modeling of spatial changes in HF through heterogeneous TT reorganization and RyR2 orphaning (5000 of 20 000 CRUs) uncovered a local mechanism of delayed subcellular Ca2+ release and action potential prolongation. Conclusions: This study introduces STED nanoscopy for live mapping of TT membrane structures. During early HF development, the local TT morphology and associated proteins were significantly altered, leading to differential network remodeling and Ca2+ release dyssynchrony. Our data suggest that TT remodeling during HF development involves proliferative membrane changes, early excitation-contraction uncoupling, and network fracturing."],["dc.identifier.doi","10.1161/CIRCRESAHA.112.274530"],["dc.identifier.gro","3142487"],["dc.identifier.isi","000307308700007"],["dc.identifier.pmid","22723297"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8829"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/73"],["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 | A05: Molekulares Imaging von kardialen Calcium-Freisetzungsdomänen"],["dc.relation","SFB 1002 | A09: Lokale molekulare Nanodomänen-Regulation der kardialen Ryanodin-Rezeptor-Funktion"],["dc.relation.issn","0009-7330"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Hell"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Luther (Biomedical Physics)"],["dc.title","Stimulated Emission Depletion Live-Cell Super-Resolution Imaging Shows Proliferative Remodeling of T-Tubule Membrane Structures After Myocardial Infarction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","267a"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Brandenburg, Sören"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Williams, George S.B."],["dc.contributor.author","Gusev, Konstantin"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Hebisch, Elke"],["dc.contributor.author","Ward, Christopher W."],["dc.contributor.author","Lederer, W.J."],["dc.contributor.author","Lehnart, Stephan E."],["dc.date.accessioned","2020-12-10T14:22:41Z"],["dc.date.available","2020-12-10T14:22:41Z"],["dc.date.issued","2016"],["dc.format.extent","267A"],["dc.identifier.doi","10.1016/j.bpj.2015.11.1454"],["dc.identifier.isi","000375141600298"],["dc.identifier.issn","0006-3495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71697"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.publisher.place","Cambridge"],["dc.relation.eventlocation","Los Angeles, CA"],["dc.relation.issn","1542-0086"],["dc.relation.issn","0006-3495"],["dc.title","Axial Membrane Tubules in Atrial Cardiomyocytes Confine Ultrarapid Intracellular Calcium Signals through a New Super-Hub Mechanism"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e51823"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","92"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.bibliographiccitation.lastpage","19"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Brandenburg, Sören"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Lehnart, Stephan Elmar"],["dc.date.accessioned","2018-05-07T12:58:36Z"],["dc.date.available","2018-05-07T12:58:36Z"],["dc.date.issued","2014"],["dc.description.abstract","In cardiac myocytes a complex network of membrane tubules--the transverse-axial tubule system (TATS)--controls deep intracellular signaling functions. While the outer surface membrane and associated TATS membrane components appear to be continuous, there are substantial differences in lipid and protein content. In ventricular myocytes (VMs), certain TATS components are highly abundant contributing to rectilinear tubule networks and regular branching 3D architectures. It is thought that peripheral TATS components propagate action potentials from the cell surface to thousands of remote intracellular sarcoendoplasmic reticulum (SER) membrane contact domains, thereby activating intracellular Ca(2+) release units (CRUs). In contrast to VMs, the organization and functional role of TATS membranes in atrial myocytes (AMs) is significantly different and much less understood. Taken together, quantitative structural characterization of TATS membrane networks in healthy and diseased myocytes is an essential prerequisite towards better understanding of functional plasticity and pathophysiological reorganization. Here, we present a strategic combination of protocols for direct quantitative analysis of TATS membrane networks in living VMs and AMs. For this, we accompany primary cell isolations of mouse VMs and/or AMs with critical quality control steps and direct membrane staining protocols for fluorescence imaging of TATS membranes. Using an optimized workflow for confocal or superresolution TATS image processing, binarized and skeletonized data are generated for quantitative analysis of the TATS network and its components. Unlike previously published indirect regional aggregate image analysis strategies, our protocols enable direct characterization of specific components and derive complex physiological properties of TATS membrane networks in living myocytes with high throughput and open access software tools. In summary, the combined protocol strategy can be readily applied for quantitative TATS network studies during physiological myocyte adaptation or disease changes, comparison of different cardiac or skeletal muscle cell types, phenotyping of transgenic models, and pharmacological or therapeutic interventions."],["dc.identifier.doi","10.3791/51823"],["dc.identifier.pmid","25350293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/14630"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/69"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A05: Molekulares Imaging von kardialen Calcium-Freisetzungsdomänen"],["dc.relation","SFB 1002 | A09: Lokale molekulare Nanodomänen-Regulation der kardialen Ryanodin-Rezeptor-Funktion"],["dc.relation.doi","10.3791/51823"],["dc.relation.eissn","1940-087X"],["dc.relation.issn","1940-087X"],["dc.relation.workinggroup","RG Brandenburg"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.title","Analysis of tubular membrane networks in cardiac myocytes from atria and ventricles"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","429a"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Gotthardt, Michael"],["dc.contributor.author","Rudolph, Franziska"],["dc.contributor.author","Huettemeister, Judith"],["dc.contributor.author","da Sliva Lopes, Katharina"],["dc.contributor.author","Yu, Lily"],["dc.contributor.author","Bergmann, Nora"],["dc.contributor.author","Fink, Claudia"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Lehnart, Stephan"],["dc.contributor.author","Gregorio, Carol"],["dc.date.accessioned","2020-12-10T14:22:43Z"],["dc.date.available","2020-12-10T14:22:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.bpj.2016.11.2293"],["dc.identifier.issn","0006-3495"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71704"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","From Ribosome to Sarcomere - Titin Dynamics in Striated Muscle Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","305"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Haematology"],["dc.bibliographiccitation.lastpage","317"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Shahnaz Syed Abd Kadir, Sharifah"],["dc.contributor.author","Christopeit, Maximilian"],["dc.contributor.author","Wulf, Gerald"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Bornhauser, Martin"],["dc.contributor.author","Schroeder, Thomas"],["dc.contributor.author","Crysandt, Martina"],["dc.contributor.author","Mayer, Karin"],["dc.contributor.author","Jonas, Julia"],["dc.contributor.author","Stelljes, Matthias"],["dc.contributor.author","Badbaran, Anita"],["dc.contributor.author","Ayuketang Ayuk, Francis"],["dc.contributor.author","Triviai, Ioanna"],["dc.contributor.author","Wolf, Dominik"],["dc.contributor.author","Wolschke, Christine"],["dc.contributor.author","Kröger, Nicolaus"],["dc.date.accessioned","2020-12-10T18:28:24Z"],["dc.date.available","2020-12-10T18:28:24Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1111/ejh.13099"],["dc.identifier.issn","0902-4441"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76342"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Impact of ruxolitinib pretreatment on outcomes after allogeneic stem cell transplantation in patients with myelofibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","82"],["dc.bibliographiccitation.journal","Biomaterials"],["dc.bibliographiccitation.lastpage","91"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Godier-Furnemont, Amandine F. G."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Laemmle, Simon"],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Vunjak-Novakovic, Gordana"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:43:40Z"],["dc.date.available","2017-09-07T11:43:40Z"],["dc.date.issued","2015"],["dc.description.abstract","A hallmark of mature mammalian ventricular myocardium is a positive force-frequency relationship (FFR). Despite evidence of organotypic structural and molecular maturation, a positive FFR has not been observed in mammalian tissue engineered heart muscle. We hypothesized that concurrent mechanical and electrical stimulation at frequencies matching physiological heart rate will result in functional maturation. We investigated the role of biomimetic mechanical and electrical stimulation in functional maturation in engineered heart muscle (EHM). Following tissue consolidation, EHM were subjected to electrical field stimulation at 0, 2, 4, or 6 Hz for 5 days, while strained on flexible poles to facilitate auxotonic contractions. EHM stimulated at 2 and 4 Hz displayed a similarly enhanced inotropic reserve, but a clearly diverging FFR. The positive FFR in 4 Hz stimulated EHM was associated with reduced calcium sensitivity, frequency-dependent acceleration of relaxation, and enhanced post-rest potentiation. This was paralleled on the cellular level with improved calcium storage and release capacity of the sarcoplasmic reticulum and enhanced T-tubulation. We conclude that electro-mechanical stimulation at a physiological frequency supports functional maturation in mammalian EHM. The observed positive FFR in EHM has important implications for the applicability of EHM in cardiovascular research. (C) 2015 Published by Elsevier Ltd."],["dc.identifier.doi","10.1016/j.biomaterials.2015.03.055"],["dc.identifier.gro","3141856"],["dc.identifier.isi","000356737800009"],["dc.identifier.pmid","25985155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1834"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/86"],["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 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | A05: Molekulares Imaging von kardialen Calcium-Freisetzungsdomänen"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","1878-5905"],["dc.relation.issn","0142-9612"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Physiologic force-frequency response in engineered heart muscle by electromechanical stimulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3999"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","4015"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Brandenburg, Sören"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Williams, George S. B."],["dc.contributor.author","Gusev, Konstantin"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Rog-Zielinska, Eva A."],["dc.contributor.author","Hebisch, Elke"],["dc.contributor.author","Dura, Miroslav"],["dc.contributor.author","Didié, Michael"],["dc.contributor.author","Gotthardt, Michael"],["dc.contributor.author","Nikolaev, Viacheslav O."],["dc.contributor.author","Kohl, Peter"],["dc.contributor.author","Ward, Christopher W."],["dc.contributor.author","Lederer, W. Jonathan"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2020-12-10T18:38:18Z"],["dc.date.available","2020-12-10T18:38:18Z"],["dc.date.issued","2016"],["dc.description.abstract","The canonical atrial myocyte (AM) is characterized by sparse transverse tubule (TT) invaginations and slow intracellular Ca2+ propagation but exhibits rapid contractile activation that is susceptible to loss of function during hypertrophic remodeling. Here, we have identified a membrane structure and Ca2+-signaling complex that may enhance the speed of atrial contraction independently of phospholamban regulation. This axial couplon was observed in human and mouse atria and is composed of voluminous axial tubules (ATs) with extensive junctions to the sarcoplasmic reticulum (SR) that include ryanodine receptor 2 (RyR2) clusters. In mouse AM, AT structures triggered Ca2+ release from the SR approximately 2 times faster at the AM center than at the surface. Rapid Ca2+ release correlated with colocalization of highly phosphorylated RyR2 clusters at AT-SR junctions and earlier, more rapid shortening of central sarcomeres. In contrast, mice expressing phosphorylation-incompetent RyR2 displayed depressed AM sarcomere shortening and reduced in vivo atrial contractile function. Moreover, left atrial hypertrophy led to AT proliferation, with a marked increase in the highly phosphorylated RyR2-pS2808 cluster fraction, thereby maintaining cytosolic Ca2+ signaling despite decreases in RyR2 cluster density and RyR2 protein expression. AT couplon \"super-hubs\" thus underlie faster excitation-contraction coupling in health as well as hypertrophic compensatory adaptation and represent a structural and metabolic mechanism that may contribute to contractile dysfunction and arrhythmias."],["dc.identifier.doi","10.1172/JCI88241"],["dc.identifier.gro","3141610"],["dc.identifier.isi","000384703300035"],["dc.identifier.pmid","27643434"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77268"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/151"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["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 | A09: Lokale molekulare Nanodomänen-Regulation der kardialen Ryanodin-Rezeptor-Funktion"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation","SFB 1002 | S02: Hochauflösende Fluoreszenzmikroskopie und integrative Datenanalyse"],["dc.relation","SFB 1002 | Z: Zentrale Organisation und Verwaltung"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG Brandenburg"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Nikolaev (Cardiovascular Research Center)"],["dc.title","Axial tubule junctions control rapid calcium signaling in atria"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","340a"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biophysical Journal"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Kohl, Tobias"],["dc.contributor.author","Wagner, Eva"],["dc.contributor.author","Brandenburg, Soeren"],["dc.contributor.author","Parlitz, Ulrich"],["dc.contributor.author","Lederer, W.J."],["dc.contributor.author","Lehnart, Stephan E."],["dc.date.accessioned","2022-03-01T11:44:56Z"],["dc.date.available","2022-03-01T11:44:56Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.bpj.2012.11.1891"],["dc.identifier.pii","S0006349512031372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103167"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0006-3495"],["dc.title","Principles of Network Organization of T-Tubule Membranes in Health and Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]