Zelarayan, Laura Cecilia

[["dc.bibliographiccitation.artnumber","P4479"],["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","suppl_1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Iyer, L. M."],["dc.contributor.author","Noack, C."],["dc.contributor.author","Nagarajan, S."],["dc.contributor.author","Woelfer, M."],["dc.contributor.author","Schoger, E."],["dc.contributor.author","Pang, S. T."],["dc.contributor.author","Kari, V."],["dc.contributor.author","Zafeiriou, M. P."],["dc.contributor.author","Toischer, K."],["dc.contributor.author","Hasenfuss, G."],["dc.contributor.author","Johnsen, S. A."],["dc.contributor.author","Zelarayan, L. C."],["dc.date.accessioned","2019-02-19T13:47:43Z"],["dc.date.available","2019-02-19T13:47:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/eurheartj/ehx504.P4479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57586"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/177"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.issn","0195-668X"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","B-catenin/TCF7L2 signaling orchestrates initiation of pathological hypertrophic cardiac remodeling by inducing chromatin modifications"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","4091"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Sitte, Maren"],["dc.contributor.author","Schmidt, Julia"],["dc.contributor.author","Parbin, Sabnam"],["dc.contributor.author","Ludewig, Fabian"],["dc.contributor.author","Yigit, Gökhan"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Wollnik, Bernd"],["dc.contributor.author","Salinas, Gabriella"],["dc.date.accessioned","2022-04-01T10:01:43Z"],["dc.date.available","2022-04-01T10:01:43Z"],["dc.date.issued","2022"],["dc.description.abstract","Single cell multi-omics analysis has the potential to yield a comprehensive understanding of the cellular events that underlie the basis of human diseases. The cardinal feature to access this information is the technology used for single-cell isolation, barcoding, and sequencing. Most currently used single-cell RNA-sequencing platforms have limitations in several areas including cell selection, documentation and library chemistry. In this study, we describe a novel high-throughput, full-length, single-cell RNA-sequencing approach that combines the CellenONE isolation and sorting system with the ICELL8 processing instrument. This method offers substantial improvements in single cell selection, documentation and capturing rate. Moreover, it allows the use of flexible chemistry for library preparations and the analysis of living or fixed cells, whole cells independent of sizing and morphology, as well as of nuclei. We applied this method to dermal fibroblasts derived from six patients with different segmental progeria syndromes and defined phenotype associated pathway signatures with variant associated expression modifiers. These results validate the applicability of our method to highlight genotype-expression relationships for molecular phenotyping of individual cells derived from human patients."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1038/s41598-022-07874-1"],["dc.identifier.pii","7874"],["dc.identifier.pmid","35260714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105735"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/460"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/424"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation.eissn","2045-2322"],["dc.relation.workinggroup","RG Wollnik"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A novel single-cell RNA-sequencing approach and its applicability connecting genotype to phenotype in ageing disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","361"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids"],["dc.bibliographiccitation.lastpage","369"],["dc.bibliographiccitation.volume","1811"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Nigam, Santosh"],["dc.contributor.author","Siafaka-Kapadai, Athanassia"],["dc.date.accessioned","2018-11-07T08:55:31Z"],["dc.date.available","2018-11-07T08:55:31Z"],["dc.date.issued","2011"],["dc.description.abstract","Pancreatic beta-cells have a deficit of scavenging enzymes such as catalase (Cat) and glutathione peroxidase (GPx) and therefore are susceptible to oxidative stress and apoptosis. Our previous work showed that, in the absence of cytosolic GPx in insulinoma RINm5F cells, an intrinsic activity of 12 lipoxygenase (12(S)-LOX) converts 12S-hydroperoxyeicosatetraenoic acid (12(S)-HpETE) to the bioactive epoxide hepoxilin A(3) (HXA(3)). The aim of the present study was to investigate the effect of HXA(3) on apoptosis as compared to its precursor 12(S)-HpETE and shed light upon the underlying pathways. In contrast to 12(S)-HpETE, which induced apoptosis via the extrinsic pathway, we found HXA(3) not only to prevent it but also to promote cell proliferation. In particular, HXA3 suppressed the pro-apoptotic BAX and upregulated the anti-apoptotic Bcl-2. Moreover, HXA(3) induced the anti-apoptotic 12(S)-LOX by recruiting heat shock protein 90 (HSP90), another anti-apoptotic protein. Finally, a co-chaperone protein of HSP90, protein phosphatase 5 (PP5), was upregulated by HXA(3), which counteracted oxidative stress-induced apoptosis by dephosphorylating and thus inactivating apoptosis signal-regulating kinase 1 (ASK1). Taken together, these findings suggest that HXA(3) protects insulinoma cells from oxidative stress and, via multiple signaling pathways, prevents them from undergoing apoptosis. (C) 2011 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft, Bonn [Ni242/27-1]"],["dc.identifier.doi","10.1016/j.bbalip.2011.03.002"],["dc.identifier.isi","000291192600001"],["dc.identifier.pmid","21420506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22928"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1388-1981"],["dc.title","Hepoxilin A(3) protects beta-cells from apoptosis in contrast to its precursor, 12-hydroperoxyeicosatetraenoic acid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","S1"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Zelarayan, Laura"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Regitz‐Zagrosek, Vera"],["dc.date.accessioned","2021-12-08T12:27:38Z"],["dc.date.available","2021-12-08T12:27:38Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1096/fasebj.29.1_supplement.966.1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95409"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","In C57Bl/6N Female Mice 17β‐Estradiol Leads to Cardiac Mass and Function Loss via a β‐Catenin Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.journal","Progress in Biophysics and Molecular Biology"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","144"],["dc.contributor.author","Schlick, Susanne F."],["dc.contributor.author","Spreckelsen, Florian"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Zelarayan, Laura C."],["dc.contributor.author","Luther, Stefan"],["dc.contributor.author","Parlitz, Ulrich"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Rehfeldt, Florian"],["dc.date.accessioned","2020-12-10T15:20:42Z"],["dc.date.available","2020-12-10T15:20:42Z"],["dc.date.issued","2019"],["dc.description.abstract","Cardiomyocyte and stroma cell cross-talk is essential for the formation of collagen-based engineered heart muscle, including engineered human myocardium (EHM). Fibroblasts are a main component of the myocardial stroma. We hypothesize that fibroblasts, by compacting the surrounding collagen network, support the self-organization of cardiomyocytes into a functional syncytium. With a focus on early self-organization processes in EHM, we studied the molecular and biophysical adaptations mediated by defined populations of fibroblasts and embryonic stem cell-derived cardiomyocytes in a collagen type I hydrogel. After a short phase of cell-independent collagen gelation (30 min), tissue compaction was progressively mediated by fibroblasts. Fibroblast-mediated tissue stiffening was attenuated in the presence of cardiomyocytes allowing for the assembly of stably contracting, force-generating EHM within 4 weeks. Comparative RNA-sequencing data corroborated that fibroblasts are particularly sensitive to the tissue compaction process, resulting in the fast activation of transcription profiles, supporting heart muscle development and extracellular matrix synthesis. Large amplitude oscillatory shear (LAOS) measurements revealed nonlinear strain stiffening at physiological strain amplitudes (>2%), which was reduced in the presence of cells. The nonlinear stress-strain response could be characterized by a mathematical model. Collectively, our study defines the interplay between fibroblasts and cardiomyocytes during human heart muscle self-organization in vitro and underscores the relevance of fibroblasts in the biological engineering of a cardiomyogenesis-supporting viscoelastic stroma. We anticipate that the established mathematical model will facilitate future attempts to optimize EHM for in vitro (disease modelling) and in vivo applications (heart repair)."],["dc.identifier.doi","10.1016/j.pbiomolbio.2018.11.011"],["dc.identifier.pmid","30553553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72769"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/248"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["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.workinggroup","RG Luther (Biomedical Physics)"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 4.0"],["dc.title","Agonistic and antagonistic roles of fibroblasts and cardiomyocytes on viscoelastic stiffening of engineered human myocardium"],["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","741"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Weber, Pamina"],["dc.contributor.author","Baltus, Doris"],["dc.contributor.author","Jatho, Aline"],["dc.contributor.author","Drews, Oliver"],["dc.contributor.author","Zelarayan, Laura C."],["dc.contributor.author","Wieland, Thomas"],["dc.contributor.author","Lutz, Susanne"],["dc.date.accessioned","2021-06-01T09:42:32Z"],["dc.date.available","2021-06-01T09:42:32Z"],["dc.date.issued","2021"],["dc.description.abstract","The Rho guanine nucleotide exchange factor RhoGEF17 was described to reside in adherens junctions (AJ) in endothelial cells (EC) and to play a critical role in the regulation of cell adhesion and barrier function. The purpose of this study was to analyze signal cascades and processes occurring subsequent to AJ disruption induced by RhoGEF17 knockdown. Primary human and immortalized rat EC were used to demonstrate that an adenoviral-mediated knockdown of RhoGEF17 resulted in cell rounding and an impairment in spheroid formation due to an enhanced proteasomal degradation of AJ components. In contrast, β-catenin degradation was impaired, which resulted in an induction of the β-catenin-target genes cyclin D1 and survivin. RhoGEF17 depletion additionally inhibited cell adhesion and sheet migration. The RhoGEF17 knockdown prevented the cells with impeded cell–cell and cell–matrix contacts from apoptosis, which was in line with a reduction in pro-caspase 3 expression and an increase in Akt phosphorylation. Nevertheless, the cells were not able to proliferate as a cell cycle block occurred. In summary, we demonstrate that a loss of RhoGEF17 disturbs cell–cell and cell–substrate interaction in EC. Moreover, it prevents the EC from cell death and blocks cell proliferation. Non-canonical β-catenin signaling and Akt activation could be identified as a potential mechanism."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cells10040741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85279"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/391"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C02: RhoGTPasen und ihre Bedeutung für die Last-abhängige Myokardfibrose"],["dc.relation.eissn","2073-4409"],["dc.relation.workinggroup","RG Lutz (G Protein-Coupled Receptor Mediated Signaling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","RhoGEF17—An Essential Regulator of Endothelial Cell Death and Growth"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.journal","Stem Cell Research"],["dc.bibliographiccitation.lastpage","131"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Haupt, Luis Peter"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Streckfuss-Bömeke, Katrin"],["dc.contributor.author","Zelarayán, Laura Cecilia"],["dc.date.accessioned","2018-04-23T11:49:22Z"],["dc.date.available","2018-04-23T11:49:22Z"],["dc.date.issued","2017"],["dc.description.abstract","Krueppel-like factor 15 (KLF15) is abundantly expressed in liver, kidney, and muscle, including myocardium. In the adult heart KLF15 is important to maintain homeostasis and to repress hypertrophic remodeling. We generated a homozygous hESC KLF15 knockout (KO) line using paired CRISPR/Cas9n. KLF15-KO cells maintained full pluripotency and differentiation potential as well as genomic integrity. We demonstrated that KLF15-KO cells can be differentiated into morphologically normal cardiomyocytes turning them into a valuable tool for studying human KLF15-mediated mechanisms resulting in human cardiac dysfunction."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1016/j.scr.2017.07.007"],["dc.identifier.gro","3142524"],["dc.identifier.pmid","28925362"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14618"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13680"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/175"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.issn","1873-5061"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Generation of a KLF15 homozygous knockout human embryonic stem cell line using paired CRISPR/Cas9n, and human cardiomyocytes derivation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1537"],["dc.bibliographiccitation.issue","6562"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","1540"],["dc.bibliographiccitation.volume","373"],["dc.contributor.author","Chen, Yanpu"],["dc.contributor.author","Lüttmann, Felipe F."],["dc.contributor.author","Schoger, Eric"],["dc.contributor.author","Schöler, Hans R."],["dc.contributor.author","Zelarayán, Laura C."],["dc.contributor.author","Kim, Kee-Pyo"],["dc.contributor.author","Haigh, Jody J."],["dc.contributor.author","Kim, Johnny"],["dc.contributor.author","Braun, Thomas"],["dc.date.accessioned","2021-10-01T09:58:23Z"],["dc.date.available","2021-10-01T09:58:23Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1126/science.abg5159"],["dc.identifier.pmid","34554778"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90052"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/404"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","Reversible reprogramming of cardiomyocytes to a fetal state drives heart regeneration in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Schaeffer, Hans-Joerg"],["dc.contributor.author","Bergmann, Martin"],["dc.contributor.author","Zelarayan, Laura"],["dc.date.accessioned","2018-11-07T08:49:44Z"],["dc.date.available","2018-11-07T08:49:44Z"],["dc.date.issued","2011"],["dc.identifier.isi","000299738706353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21532"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0009-7322"],["dc.title","Interaction of Krueppel-Like Factor (klf) 15 and Wnt-Signaling Pathway and its Role in Adult Cardiac Precursor Cell Regulation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Jarry, Hubertus"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.date.accessioned","2018-11-07T09:57:25Z"],["dc.date.available","2018-11-07T09:57:25Z"],["dc.date.issued","2015"],["dc.format.extent","247"],["dc.identifier.isi","000366200402401"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37151"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Loss of cardiac mass and function induced by 17beta-oestradiol via a beta-catenin mechanism in C57Bl/6N female mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]