Now showing 1 - 10 of 29
  • 2017Journal Article Research Paper
    [["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"]]
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  • 2011Journal Article
    [["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"]]
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  • 2011Conference Abstract
    [["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"]]
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  • 2020Journal Article Research Paper
    [["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.contributor.author","Rathjens, Franziska S."],["dc.contributor.author","Blenkle, Alica"],["dc.contributor.author","Iyer, Lavanya M."],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Syeda, Fahima"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Jungmann, Andreas"],["dc.contributor.author","Dewenter, Matthias"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.date.accessioned","2021-06-01T10:51:17Z"],["dc.date.available","2021-06-01T10:51:17Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Aims  Arrhythmias and sudden cardiac death (SCD) occur commonly in patients with heart failure. We found T-box 5 (TBX5) dysregulated in ventricular myocardium from heart failure patients and thus we hypothesized that TBX5 reduction contributes to arrhythmia development in these patients. To understand the underlying mechanisms, we aimed to reveal the ventricular TBX5-dependent transcriptional network and further test the therapeutic potential of TBX5 level normalization in mice with documented arrhythmias. Methods and results  We used a mouse model of TBX5 conditional deletion in ventricular cardiomyocytes. Ventricular (v) TBX5 loss in mice resulted in mild cardiac dysfunction and arrhythmias and was associated with a high mortality rate (60%) due to SCD. Upon angiotensin stimulation, vTbx5KO mice showed exacerbated cardiac remodelling and dysfunction suggesting a cardioprotective role of TBX5. RNA-sequencing of a ventricular-specific TBX5KO mouse and TBX5 chromatin immunoprecipitation was used to dissect TBX5 transcriptional network in cardiac ventricular tissue. Overall, we identified 47 transcripts expressed under the control of TBX5, which may have contributed to the fatal arrhythmias in vTbx5KO mice. These included transcripts encoding for proteins implicated in cardiac conduction and contraction (Gja1, Kcnj5, Kcng2, Cacna1g, Chrm2), in cytoskeleton organization (Fstl4, Pdlim4, Emilin2, Cmya5), and cardiac protection upon stress (Fhl2, Gpr22, Fgf16). Interestingly, after TBX5 loss and arrhythmia development in vTbx5KO mice, TBX5 protein-level normalization by systemic adeno-associated-virus (AAV) 9 application, re-established TBX5-dependent transcriptome. Consequently, cardiac dysfunction was ameliorated and the propensity of arrhythmia occurrence was reduced. Conclusions  This study uncovers a novel cardioprotective role of TBX5 in the adult heart and provides preclinical evidence for the therapeutic value of TBX5 protein normalization in the control of arrhythmia."],["dc.identifier.doi","10.1093/cvr/cvaa239"],["dc.identifier.pmid","32777030"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86956"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/211"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/380"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["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.eissn","1755-3245"],["dc.relation.issn","0008-6363"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY-NC 4.0"],["dc.title","Preclinical evidence for the therapeutic value of TBX5 normalization in arrhythmia control"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","389"],["dc.contributor.author","Schoger, E."],["dc.contributor.author","Chebbok, E."],["dc.contributor.author","Noack, C."],["dc.contributor.author","Zafiriou, M.-P."],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2018-11-07T10:19:01Z"],["dc.date.available","2018-11-07T10:19:01Z"],["dc.date.issued","2016"],["dc.format.extent","S41"],["dc.identifier.isi","000398368200165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41574"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","82nd Annual Meeting of the German-Society-for-Exerimental-and-Clinical-Pharmacology-and-Toxicology (DGPT) / 18th Annual Meeting of the Network-Clinical-Pharmacology-Germany (VKliPha)"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1432-1912"],["dc.relation.issn","0028-1298"],["dc.title","Characterization of Basic Leucine Zipper and W2 Domain Containing Protein 2 (BZW2), a novel Wnt component"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","992"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1007"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Schaeffer, Hans-Joerg"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2017-09-07T11:48:25Z"],["dc.date.available","2017-09-07T11:48:25Z"],["dc.date.issued","2012"],["dc.description.abstract","Wnt/beta-catenin signalling controls adult heart remodelling in part via regulation of cardiac progenitor cell (CPC) differentiation. An enhanced understanding of mechanisms controlling CPC biology might facilitate the development of new therapeutic strategies in heart failure. We identified and characterized a novel cardiac interaction between Krueppel-like factor 15 and components of the Wnt/beta-catenin pathway leading to inhibition of transcription. In vitro mutation, reporter assays and co-localization analyses revealed that KLF15 requires both the C-terminus, necessary for nuclear localization, and a minimal N-terminal regulatory region to inhibit transcription. In line with this, functional Klf15 knock-out mice exhibited cardiac beta-catenin transcriptional activation along with functional cardiac deterioration in normal homeostasis and upon hypertrophy. We further provide in vivo and in vitro evidences for preferential endothelial lineage differentiation of CPCs upon KLF15 deletion. Via inhibition of beta-catenin transcription, KLF15 controls CPC homeostasis in the adult heart similar to embryonic cardiogenesis. This knowledge may provide a tool for reactivation of this apparently dormant CPC population in the adult heart and thus be an attractive approach to enhance endogenous cardiac repair."],["dc.identifier.doi","10.1002/emmm.201101043"],["dc.identifier.gro","3142470"],["dc.identifier.isi","000308302900015"],["dc.identifier.pmid","22767436"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8640"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft (DFG); Juergen Manchot Foundation"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1757-4676"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Krueppel-like factor 15 regulates Wnt/ss-catenin transcription and controls cardiac progenitor cell fate in the postnatal heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2022-11-16Journal Article
    [["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Schmidt, Julia; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Dreha-Kulaczewski, Steffi; \n2\nDepartment of Pediatics and Adolescent Medicine, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Zafeiriou, Maria-Patapia; \n3\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schreiber, Marie-Kristin; \n3\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Wilken, Bernd; \n6\nDepartment of Pediatric Neurology, Klinikum Kassel, Kassel, Germany"],["dc.contributor.affiliation","Funke, Rudolf; \n6\nDepartment of Pediatric Neurology, Klinikum Kassel, Kassel, Germany"],["dc.contributor.affiliation","Neuhofer, Christiane M; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Altmüller, Janine; \n9\nCologne Center for Genomics (CCG), University of Cologne, Faculty of Medicine, University Hospital Cologne, Cologne, Germany"],["dc.contributor.affiliation","Thiele, Holger; \n9\nCologne Center for Genomics (CCG), University of Cologne, Faculty of Medicine, University Hospital Cologne, Cologne, Germany"],["dc.contributor.affiliation","Nürnberg, Peter; \n9\nCologne Center for Genomics (CCG), University of Cologne, Faculty of Medicine, University Hospital Cologne, Cologne, Germany"],["dc.contributor.affiliation","Biskup, Saskia; \n12\nCeGaT GmbH, Center for Genomics and Transcriptomics, Tübingen, Germany"],["dc.contributor.affiliation","Li, Yun; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Zimmermann, Wolfram Hubertus; \n3\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Kaulfuß, Silke; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Yigit, Gökhan; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Wollnik, Bernd; \n1\nInstitute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Schmidt, Julia"],["dc.contributor.author","Dreha-Kulaczewski, Steffi"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.contributor.author","Schreiber, Marie-Kristin"],["dc.contributor.author","Wilken, Bernd"],["dc.contributor.author","Funke, Rudolf"],["dc.contributor.author","Neuhofer, Christiane M"],["dc.contributor.author","Altmüller, Janine"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Biskup, Saskia"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Kaulfuß, Silke"],["dc.contributor.author","Yigit, Gökhan"],["dc.contributor.author","Wollnik, Bernd"],["dc.date.accessioned","2022-11-30T10:25:07Z"],["dc.date.available","2022-11-30T10:25:07Z"],["dc.date.issued","2022-11-16"],["dc.date.updated","2022-11-30T08:55:41Z"],["dc.description.abstract","STAG2 is a component of the large, evolutionarily highly conserved cohesin complex, which has been linked to various cellular processes like genome organization, DNA replication, gene expression, heterochromatin formation, sister chromatid cohesion, and DNA repair. A wide spectrum of germline variants in genes encoding subunits or regulators of the cohesin complex have previously been identified to cause distinct but phenotypically overlapping multisystem developmental disorders belonging to the group of cohesinopathies. Pathogenic variants in STAG2 have rarely been implicated in an X-linked cohesinopathy associated with undergrowth, developmental delay, and dysmorphic features. Here, we describe for the first time a mosaic STAG2 variant in an individual with developmental delay, microcephaly, and hemihypotrophy of the right side. We characterized the grade of mosaicism by deep sequencing analysis on DNA extracted from EDTA blood, urine and buccal swabs. Furthermore, we report an additional female with a novel de novo splice variant in STAG2. Interestingly, both individuals show supernumerary nipples, a feature that has not been reported associated to STAG2 before. Remarkably, additional analysis of STAG2 transcripts in both individuals showed only wildtype transcripts, even after blockage of nonsense-mediated decay using puromycin in blood lymphocytes. As the phenotype of STAG2-associated cohesinopathies is dominated by global developmental delay, severe microcephaly, and brain abnormalities, we investigated the expression of STAG2 and other related components of the cohesin complex during Bioengineered Neuronal Organoids (BENOs) generation by RNA sequencing. Interestingly, we observed a prominent expression of STAG2, especially between culture days 0 and 15, indicating an essential function of STAG2 in early brain development. In summary, we expand the genotypic and phenotypic spectrum of STAG2-associated cohesinopathies and show that BENOs represent a promising model to gain further insights into the critical role of STAG2 in the complex process of nervous system development."],["dc.identifier.doi","10.3389/fcell.2022.1025332"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/117901"],["dc.language.iso","en"],["dc.relation.eissn","2296-634X"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Somatic mosaicism in STAG2-associated cohesinopathies: Expansion of the genotypic and phenotypic spectrum"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2011Conference Abstract
    [["dc.bibliographiccitation.firstpage","44"],["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","383"],["dc.contributor.author","Noack, C."],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Zafiriou, M.-P."],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Schaeffer, H.-J."],["dc.contributor.author","Bergmann, M."],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2018-11-07T08:58:31Z"],["dc.date.available","2018-11-07T08:58:31Z"],["dc.date.issued","2011"],["dc.identifier.isi","000288573100216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23661"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","77th Annual Meeting on German-Society-for-Experimental-and-Clinical-Pharmacology-and-Toxicology"],["dc.relation.eventlocation","Frankfurt, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","Interaction of Kruppel-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"]]
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  • 2011Conference Abstract
    [["dc.bibliographiccitation.journal","Naunyn-Schmiedeberg s Archives of Pharmacology"],["dc.bibliographiccitation.volume","383"],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.contributor.author","Noack, C."],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Dietz, Rainer"],["dc.contributor.author","Bergmann, M."],["dc.contributor.author","Zelarayan, Laura Cecilia"],["dc.date.accessioned","2018-11-07T08:58:31Z"],["dc.date.available","2018-11-07T08:58:31Z"],["dc.date.issued","2011"],["dc.format.extent","37"],["dc.identifier.isi","000288573100178"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23660"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","77th Annual Meeting on German-Society-for-Experimental-and-Clinical-Pharmacology-and-Toxicology"],["dc.relation.eventlocation","Frankfurt, GERMANY"],["dc.relation.issn","0028-1298"],["dc.title","Expression and role of EpoR/Epo signaling in the biology of mouse cardiac progenitor cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article Erratum
    [["dc.bibliographiccitation.journal","Translational Stroke Research"],["dc.contributor.author","Zheng, X."],["dc.contributor.author","Zhang, L."],["dc.contributor.author","Kuang, Y."],["dc.contributor.author","Venkataramani, V."],["dc.contributor.author","Jin, F."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Zafeiriou, Maria Patapia"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Moebius, W."],["dc.contributor.author","Kilic, E."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-12-01T09:23:27Z"],["dc.date.available","2021-12-01T09:23:27Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1007/s12975-021-00961-x"],["dc.identifier.pii","961"],["dc.identifier.pmid","34751929"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94655"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/441"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/421"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation.eissn","1868-601X"],["dc.relation.iserratumof","/handle/2/71426"],["dc.relation.issn","1868-4483"],["dc.relation.workinggroup","RG Bähr (Neurobiological Research Laboratory)"],["dc.relation.workinggroup","RG Möbius"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Lenz"],["dc.title","Correction to: Extracellular Vesicles Derived from Neural Progenitor Cells––a Preclinical Evaluation for Stroke Treatment in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]
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