Lizé, Muriel

[["dc.bibliographiccitation.artnumber","1183"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Fuertes-Alvarez, Sandra"],["dc.contributor.author","Maeso-Alonso, Laura"],["dc.contributor.author","Villoch-Fernandez, Javier"],["dc.contributor.author","Wildung, Merit"],["dc.contributor.author","Martin-Lopez, Marta"],["dc.contributor.author","Marshall, Clayton"],["dc.contributor.author","Villena-Cortes, Alberto J."],["dc.contributor.author","Diez-Prieto, Inmaculada"],["dc.contributor.author","Pietenpol, Jennifer A."],["dc.contributor.author","Tissir, Fadel"],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Marques, Margarita M."],["dc.contributor.author","Marin, Maria C."],["dc.date.accessioned","2019-07-09T11:50:56Z"],["dc.date.available","2019-07-09T11:50:56Z"],["dc.date.issued","2018"],["dc.description.abstract","Planar cell polarity (PCP) and intercellular junctional complexes establish tissue structure and coordinated behaviors across epithelial sheets. In multiciliated ependymal cells, rotational and translational PCP coordinate cilia beating and direct cerebrospinal fluid circulation. Thus, PCP disruption results in ciliopathies and hydrocephalus. PCP establishment depends on the polarization of cytoskeleton and requires the asymmetric localization of core and global regulatory modules, including membrane proteins like Vangl1/2 or Frizzled. We analyzed the subcellular localization of select proteins that make up these modules in ependymal cells and the effect of Trp73 loss on their localization. We identify a novel function of the Trp73 tumor suppressor gene, the TAp73 isoform in particular, as an essential regulator of PCP through the modulation of actin and microtubule cytoskeleton dynamics, demonstrating that Trp73 is a key player in the organization of ependymal ciliated epithelia. Mechanistically, we show that p73 regulates translational PCP and actin dynamics through TAp73-dependent modulation of non-musclemyosin-II activity. In addition, TAp73 is required for the asymmetric localization of PCP-core and global signaling modules and regulates polarized microtubule dynamics, which in turn set up the rotational PCP. Therefore, TAp73 modulates, directly and/or indirectly, transcriptional programs regulating actin and microtubules dynamics and Golgi organization signaling pathways. These results shed light into the mechanism of ependymal cell planar polarization and reveal p73 as an epithelial architect during development regulating the cellular cytoskeleton."],["dc.identifier.doi","10.1038/s41419-018-1205-6"],["dc.identifier.pmid","30518789"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59854"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","p73 regulates ependymal planar cell polarity by modulating actin and microtubule cytoskeleton"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","452"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Lize, M."],["dc.contributor.author","Pilarski, S."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T08:45:16Z"],["dc.date.available","2018-11-07T08:45:16Z"],["dc.date.issued","2010"],["dc.description.abstract","E2F1 is a positive regulator of cell cycle progression and also a potent inducer of apoptosis, especially when activated by DNA damage. We identified E2F1-inducible microRNAs (miRNAs) by microarray hybridization and found that the levels of miRNAs 449a and 449b, as well as their host gene CDC20B, are strongly upregulated by E2F1. High miR-449 levels were found in testes, lung, and trachea, but not in testicular and other cancer cells. MiR-449a/b structurally resemble the p53-inducible miRNA 34 family. In agreement with a putative tumor-suppressive role, miR-449a as well as miR-34a reduced proliferation and strongly promoted apoptosis by at least partially p53-independent mechanisms. Both miRNAs reduced the levels of CDK6, implying miR-449 in a negative feedback mechanism for E2F1. Moreover, miR-449a and miR-34a diminished the deacetylase Sirt1 and augmented p53 acetylation. We propose that both miRNAs provide a twofold safety mechanism to avoid excessive E2F1-induced proliferation by cell cycle arrest and by apoptosis. While responding to different transactivators, miRNAs 449 and 34 each repress E2F1, but promote p53 activity, allowing efficient cross-talk between two major DNA damage-responsive gene regulators. Cell Death and Differentiation (2010) 17, 452-458; doi: 10.1038/cdd.2009.188; published online 4 December 2009"],["dc.identifier.doi","10.1038/cdd.2009.188"],["dc.identifier.isi","000274565300008"],["dc.identifier.pmid","19960022"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20395"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1350-9047"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","E2F1-inducible microRNA 449a/b suppresses cell proliferation and promotes apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","D689"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","D694"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Doenitz, Juergen"],["dc.contributor.author","Goemann, Bjoern"],["dc.contributor.author","Lize, Muriel"],["dc.contributor.author","Michael, Holger"],["dc.contributor.author","Sasse, Nicole"],["dc.contributor.author","Wingender, Edgar"],["dc.contributor.author","Potapov, Anatolij P."],["dc.date.accessioned","2018-11-07T11:20:30Z"],["dc.date.available","2018-11-07T11:20:30Z"],["dc.date.issued","2008"],["dc.description.abstract","EndoNet is an information resource about intercellular regulatory communication. It provides information about hormones, hormone receptors, the sources (i.e. cells, tissues and organs) where the hormones are synthesized and secreted, and where the respective receptors are expressed. The database focuses on the regulatory relations between them. An elementary communication is displayed as a causal link from a cell that secretes a particular hormone to those cells which express the corresponding hormone receptor and respond to the hormone. Whenever expression, synthesis and/or secretion of another hormone are part of this response, it renders the corresponding cell an internal node of the resulting network. This intercellular communication network coordinates the function of different organs. Therefore, the database covers the hierarchy of cellular organization of tissues and organs as it has been modeled in the Cytomer ontology, which has now been directly embedded into EndoNet. The user can query the database; the results can be used to visualize the intercellular information flow. A newly implemented hormone classification enables to browse the database and may be used as alternative entry point. EndoNet is accessible at: http://endonet.bioinf.med.uni-goettingen.de/."],["dc.identifier.doi","10.1093/nar/gkm940"],["dc.identifier.isi","000252545400124"],["dc.identifier.pmid","18045786"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55550"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","EndoNet: an information resource about regulatory networks of cell-to-cell communication"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","10"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Cancer : EJC Supplements"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Herr, C."],["dc.contributor.author","Bals, R."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2022-03-01T11:45:36Z"],["dc.date.available","2022-03-01T11:45:36Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/S1359-6349(10)70847-8"],["dc.identifier.pii","S1359634910708478"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103385"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","1359-6349"],["dc.title","38 miR-449 induces apoptosis while triggering a stress and DNA damage response"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7749"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","23"],["dc.contributor.affiliation","Wildung, Merit; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.affiliation","Herr, Christian; 3Department of Internal Medicine V, Saarland University, 66421 Homburg, Germany; christian.herr@uks.eu (C.H.); christoph.beisswenger@uks.eu (C.B.); m5.sekr@uks.eu (R.B.)"],["dc.contributor.affiliation","Riedel, Dietmar; 4Laboratory for Electron Microscopy, Max Planck Institute for Multidisciplinary Sciences, 37075 Goettingen, Germany; driedel@mpinat.mpg.de"],["dc.contributor.affiliation","Wiedwald, Cornelia; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.affiliation","Moiseenko, Alena; 5Immunology & Respiratory Department, Boehringer Ingelheim Pharma GmbH, 88400 Biberach an der Riss, Germany; alena.moiseenko@boehringer-ingelheim.com"],["dc.contributor.affiliation","Ramírez, Fidel; 6Global Computational Biology and Digital Sciences Department, Boehringer Ingelheim Pharma GmbH, 88400 Biberach an der Riss, Germany; fidel.ramirez@boehringer-ingelheim.com"],["dc.contributor.affiliation","Tasena, Hataitip; 7Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9712 Groningen, The Netherlands; h.tasena@nus.edu.sg (H.T.); w.timens@umcg.nl (W.T.); c.a.brandsma@umcg.nl (C.-A.B.); h.i.heijink@umcg.nl (I.H.H.)"],["dc.contributor.affiliation","Heimerl, Maren; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.affiliation","Alevra, Mihai; 9Institute of Neuro- and Sensory Physiology, Goettingen University, 37073 Goettingen, Germany; malevra@gwdg.de"],["dc.contributor.affiliation","Movsisyan, Naira; 10Oncophysiology Group, Max Planck Institute for Multidisciplinary Sciences, 37075 Goettingen, Germany; nairamovsisian@gmail.com (N.M.); urrego.dianae@gmail.com (D.U.); pardo@mpinat.mpg.de (L.A.P.)"],["dc.contributor.affiliation","Schuldt, Maike; 2Molecular Oncology, University Medical Center Goettingen, 37077 Goettingen, Germany; maikeschuldt@web.de (M.S.); bernard.freytag@stud.uni-goettingen.de (B.F.)"],["dc.contributor.affiliation","Volceanov-Hahn, Larisa; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.affiliation","Provoost, Sharen; 11Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, 9000 Ghent, Belgium; sharenprovoost@hotmail.com (S.P.); tania.maes@ugent.be (T.M.)"],["dc.contributor.affiliation","Nöthe-Menchen, Tabea; 12Department of General Pediatrics, University Hospital Muenster, 48149 Muenster, Germany; tabea.noethe-menchen@ukmuenster.de (T.N.-M.); julia.wallmeier@ukmuenster.de (J.W.)"],["dc.contributor.affiliation","Urrego, Diana; 10Oncophysiology Group, Max Planck Institute for Multidisciplinary Sciences, 37075 Goettingen, Germany; nairamovsisian@gmail.com (N.M.); urrego.dianae@gmail.com (D.U.); pardo@mpinat.mpg.de (L.A.P.)"],["dc.contributor.affiliation","Freytag, Bernard; 2Molecular Oncology, University Medical Center Goettingen, 37077 Goettingen, Germany; maikeschuldt@web.de (M.S.); bernard.freytag@stud.uni-goettingen.de (B.F.)"],["dc.contributor.affiliation","Wallmeier, Julia; 12Department of General Pediatrics, University Hospital Muenster, 48149 Muenster, Germany; tabea.noethe-menchen@ukmuenster.de (T.N.-M.); julia.wallmeier@ukmuenster.de (J.W.)"],["dc.contributor.affiliation","Beisswenger, Christoph; 3Department of Internal Medicine V, Saarland University, 66421 Homburg, Germany; christian.herr@uks.eu (C.H.); christoph.beisswenger@uks.eu (C.B.); m5.sekr@uks.eu (R.B.)"],["dc.contributor.affiliation","Bals, Robert; 3Department of Internal Medicine V, Saarland University, 66421 Homburg, Germany; christian.herr@uks.eu (C.H.); christoph.beisswenger@uks.eu (C.B.); m5.sekr@uks.eu (R.B.)"],["dc.contributor.affiliation","van den Berge, Maarten; 8Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, 9712 Groningen, The Netherlands; m.van.den.berge@umcg.nl"],["dc.contributor.affiliation","Timens, Wim; 7Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9712 Groningen, The Netherlands; h.tasena@nus.edu.sg (H.T.); w.timens@umcg.nl (W.T.); c.a.brandsma@umcg.nl (C.-A.B.); h.i.heijink@umcg.nl (I.H.H.)"],["dc.contributor.affiliation","Hiemstra, Pieter S.; 14Department of Pulmonology, Leiden University Medical Centre, 2333 Leiden, The Netherlands; p.s.hiemstra@lumc.nl"],["dc.contributor.affiliation","Brandsma, Corry-Anke; 7Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9712 Groningen, The Netherlands; h.tasena@nus.edu.sg (H.T.); w.timens@umcg.nl (W.T.); c.a.brandsma@umcg.nl (C.-A.B.); h.i.heijink@umcg.nl (I.H.H.)"],["dc.contributor.affiliation","Maes, Tania; 11Laboratory for Translational Research in Obstructive Pulmonary Diseases, Department of Respiratory Medicine, Ghent University Hospital, 9000 Ghent, Belgium; sharenprovoost@hotmail.com (S.P.); tania.maes@ugent.be (T.M.)"],["dc.contributor.affiliation","Andreas, Stefan; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.affiliation","Heijink, Irene H.; 7Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, 9712 Groningen, The Netherlands; h.tasena@nus.edu.sg (H.T.); w.timens@umcg.nl (W.T.); c.a.brandsma@umcg.nl (C.-A.B.); h.i.heijink@umcg.nl (I.H.H.)"],["dc.contributor.affiliation","Pardo, Luis A.; 10Oncophysiology Group, Max Planck Institute for Multidisciplinary Sciences, 37075 Goettingen, Germany; nairamovsisian@gmail.com (N.M.); urrego.dianae@gmail.com (D.U.); pardo@mpinat.mpg.de (L.A.P.)"],["dc.contributor.affiliation","Lizé, Muriel; 1Molecular & Experimental Pneumology Group, Clinic for Cardiology and Pneumology, University Medical Center Goettingen, 37075 Gottingen, Germany; meritwildung@web.de (M.W.); cornelia.wiedwald@biontech.de (C.W.); heimerl.maren@mh-hannover.de (M.H.); lvolcea@gwdg.de (L.V.-H.); stefan.andreas@med.uni-goettingen.de (S.A.)"],["dc.contributor.author","Wildung, Merit"],["dc.contributor.author","Herr, Christian"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Wiedwald, Cornelia"],["dc.contributor.author","Moiseenko, Alena"],["dc.contributor.author","Ramírez, Fidel"],["dc.contributor.author","Tasena, Hataitip"],["dc.contributor.author","Heimerl, Maren"],["dc.contributor.author","Alevra, Mihai"],["dc.contributor.author","Movsisyan, Naira"],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Schuldt, Maike"],["dc.contributor.author","Volceanov-Hahn, Larisa"],["dc.contributor.author","Provoost, Sharen"],["dc.contributor.author","Nöthe-Menchen, Tabea"],["dc.contributor.author","Urrego, Diana"],["dc.contributor.author","Freytag, Bernard"],["dc.contributor.author","Wallmeier, Julia"],["dc.contributor.author","Beisswenger, Christoph"],["dc.contributor.author","Bals, Robert"],["dc.contributor.author","van den Berge, Maarten"],["dc.contributor.author","Timens, Wim"],["dc.contributor.author","Hiemstra, Pieter S."],["dc.contributor.author","Brandsma, Corry-Anke"],["dc.contributor.author","Maes, Tania"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Heijink, Irene H."],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2022-09-01T09:51:11Z"],["dc.date.available","2022-09-01T09:51:11Z"],["dc.date.issued","2022"],["dc.date.updated","2022-09-03T22:18:07Z"],["dc.description.abstract","Airway mucociliary regeneration and function are key players for airway defense and are impaired in chronic obstructive pulmonary disease (COPD). Using transcriptome analysis in COPD-derived bronchial biopsies, we observed a positive correlation between cilia-related genes and microRNA-449 (miR449). In vitro, miR449 was strongly increased during airway epithelial mucociliary differentiation. In vivo, miR449 was upregulated during recovery from chemical or infective insults. miR0449−/− mice (both alleles are deleted) showed impaired ciliated epithelial regeneration after naphthalene and Haemophilus influenzae exposure, accompanied by more intense inflammation and emphysematous manifestations of COPD. The latter occurred spontaneously in aged miR449−/− mice. We identified Aurora kinase A and its effector target HDAC6 as key mediators in miR449-regulated ciliary homeostasis and epithelial regeneration. Aurora kinase A is downregulated upon miR449 overexpression in vitro and upregulated in miR449−/− mouse lungs. Accordingly, imaging studies showed profoundly altered cilia length and morphology accompanied by reduced mucociliary clearance. Pharmacological inhibition of HDAC6 rescued cilia length and coverage in miR449−/− cells, consistent with its tubulin-deacetylating function. Altogether, our study establishes a link between miR449, ciliary dysfunction, and COPD pathogenesis."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","UMG Goettingen"],["dc.description.sponsorship","EMBO"],["dc.description.sponsorship","Interdisziplinaeres Zentrum für Klinische Forschung (IZKF) Muenster"],["dc.description.sponsorship","University of Muenster Medical School"],["dc.description.sponsorship","Belgian Interuniversity Attraction Poles"],["dc.description.sponsorship","Research foundation Flanders (FWO)"],["dc.identifier.doi","10.3390/ijms23147749"],["dc.identifier.pii","ijms23147749"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113901"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.title","miR449 Protects Airway Regeneration by Controlling AURKA/HDAC6-Mediated Ciliary Disassembly"],["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","1088"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Respiratory and Critical Care Medicine"],["dc.bibliographiccitation.lastpage","1104"],["dc.bibliographiccitation.volume","202"],["dc.contributor.author","Zysman, Maéva"],["dc.contributor.author","Baptista, Bruno Ribeiro"],["dc.contributor.author","Essari, Laure-Aléa"],["dc.contributor.author","Taghizadeh, Sara"],["dc.contributor.author","Thibault de Ménonville, Charlotte"],["dc.contributor.author","Giffard, Clément"],["dc.contributor.author","Issa, Amelle"],["dc.contributor.author","Franco-Montoya, Marie-Laure"],["dc.contributor.author","Breau, Marielle"],["dc.contributor.author","Souktani, Rachid"],["dc.contributor.author","Aissat, Abdel"],["dc.contributor.author","Caeymaex, Laurence"],["dc.contributor.author","Lizé, Muriel"],["dc.contributor.author","Van Nhieu, Jeanne Tran"],["dc.contributor.author","Jung, Camille"],["dc.contributor.author","Rottier, Robert"],["dc.contributor.author","Cruzeiro, Marcio Do"],["dc.contributor.author","Adnot, Serge"],["dc.contributor.author","Epaud, Ralph"],["dc.contributor.author","Chabot, François"],["dc.contributor.author","Lanone, Sophie"],["dc.contributor.author","Boczkowski, Jorge"],["dc.contributor.author","Boyer, Laurent"],["dc.date.accessioned","2021-04-14T08:31:22Z"],["dc.date.available","2021-04-14T08:31:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1164/rccm.201908-1573OC"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83575"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1535-4970"],["dc.relation.issn","1073-449X"],["dc.title","Targeting p16 INK4a Promotes Lipofibroblasts and Alveolar Regeneration after Early-Life Injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2740"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","2757"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Wildung, Merit"],["dc.contributor.author","Esser, Tilman Uli"],["dc.contributor.author","Grausam, Katie Baker"],["dc.contributor.author","Wiedwald, Cornelia"],["dc.contributor.author","Volceanov-Hahn, Larisa"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Beuermann, Sabine"],["dc.contributor.author","Li, Li"],["dc.contributor.author","Zylla, Jessica"],["dc.contributor.author","Guenther, Ann-Kathrin"],["dc.contributor.author","Wienken, Magdalena"],["dc.contributor.author","Ercetin, Evrim"],["dc.contributor.author","Han, Zhiyuan"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Zhao, Haotian"],["dc.contributor.author","Lizé, Muriel"],["dc.date.accessioned","2020-12-10T18:09:42Z"],["dc.date.available","2020-12-10T18:09:42Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41418-019-0332-7"],["dc.identifier.eissn","1476-5403"],["dc.identifier.issn","1350-9047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73732"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Transcription factor TAp73 and microRNA-449 complement each other to support multiciliogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4579"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","4583"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lize, Muriel"],["dc.contributor.author","Herr, Christian"],["dc.contributor.author","Klimke, Alexander"],["dc.contributor.author","Bals, Robert"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T08:36:50Z"],["dc.date.available","2018-11-07T08:36:50Z"],["dc.date.issued","2010"],["dc.description.abstract","MicroRNAs of the miR-34/449 family mediate cell cycle arrest and tumor suppression. Here we show that the expression of microRNA miR-449a, unlike its paralog miR-34a, is highly tissue specific and largely restricted to pulmonary and testicular tissue. MiR-449a levels in the murine lung are particularly high shortly before and after birth, coinciding with terminal differentiation of lung epithelia. Strikingly, miR-449a is upregulated by more than 1,000-fold when epithelial cells from human airways are lifted from a liquid environment to air, allowing them to undergo mucociliary differentiation. The induction of miR-449a occurs in parallel to its host gene CDC20B and the transcription factor FoxJ1. Exposure to tobacco smoke induces a moderate further increase in the levels of miR-449a, and also miR-34a, in differentiated airway epithelia. We propose that miR-449a can serve as an exquisitely sensitive and specific biomarker for the differentiation of bronchial epithelia. Moreover, miR-449a may actively promote mucociliary differentiation through its ability to block cell cycle progression, and it may conribute to a first line of defence against genotoxic stress by its proapoptotic functions."],["dc.identifier.doi","10.4161/cc.9.22.13870"],["dc.identifier.isi","000285002800031"],["dc.identifier.pmid","21088493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18400"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","microRNA-449a levels increase by several orders of magnitude during mucociliary differentiation of airway epithelia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2874"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","2882"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Lize, Muriel"],["dc.contributor.author","Klimke, Alexander"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T08:52:42Z"],["dc.date.available","2018-11-07T08:52:42Z"],["dc.date.issued","2011"],["dc.description.abstract","The microRNAs 449a, b and c (miR-449) are potent inducers of cell death, cell cycle arrest, and/or cell differentiation. They belong to the same family as the p53-responsive microRNAs miR-34. Instead of p53, however, the cell cycle regulatory transcription factor E2F1 induces miR-449. All members of this microRNA family are capable of mediating cell cycle arrest and apoptosis and might thereby contribute to tumor suppression. Underlying mechanisms include the downregulation of histone acetyl transferases and consecutive activation of p53, but also the targeting of cyclin dependent kinases and their association partners. Thus, miR-34 and miR-449 provide an asymmetric feedback loop to balance E2F and p53 activities. More recently, it was discovered that miR-449 displays strong tissue specificity, with high levels in lung and testes. Two model systems (Xenopus embryos and cultured human cells) revealed that miR-449 is essential for the development of ciliated epithelia, and this appears to depend on miR-449-mediated modulation of the Notch signaling pathway. Here we summarize our current knowledge on cell fate determination by miR-449, and we propose future directions to explore the function of miR-449 in cell regulation and organismal development. MiR-449 helps to ensure proper cell function but also to avoid cancer, marking a close link between cell differentiation and tumor suppression."],["dc.identifier.doi","10.4161/cc.10.17.17181"],["dc.identifier.isi","000294480700022"],["dc.identifier.pmid","21857159"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22233"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","MicroRNA-449 in cell fate determination"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1300"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Genes & Development"],["dc.bibliographiccitation.lastpage","1312"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Kramer, Daniela"],["dc.contributor.author","Siller, Saul S."],["dc.contributor.author","Herr, Christian"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Pena, Tonatiuh"],["dc.contributor.author","Suazo, Cristina Gallinas"],["dc.contributor.author","Glaser, Katharina"],["dc.contributor.author","Wildung, Merit"],["dc.contributor.author","Steffen, Henrik"],["dc.contributor.author","Sriraman, Anusha"],["dc.contributor.author","Oberle, Fabian"],["dc.contributor.author","Wienken, Magdalena"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Vidal, Ramon"],["dc.contributor.author","Royen, Bettina"],["dc.contributor.author","Alevra, Mihai"],["dc.contributor.author","Schild, Detlev"],["dc.contributor.author","Bals, Robert"],["dc.contributor.author","Doenitz, Juergen"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Takemaru, Ken-Ichi"],["dc.contributor.author","Moll, Ute M."],["dc.contributor.author","Lize, Muriel"],["dc.date.accessioned","2018-11-07T10:13:24Z"],["dc.date.available","2018-11-07T10:13:24Z"],["dc.date.issued","2016"],["dc.description.abstract","Motile multiciliated cells (MCCs) have critical roles in respiratory health and disease and are essential for cleaning inhaled pollutants and pathogens from airways. Despite their significance for human disease, the transcriptional control that governs multiciliogenesis remains poorly understood. Here we identify TP73, a p53 homolog, as governing the program for airway multiciliogenesis. Mice with TP73 deficiency suffer from chronic respiratory tract infections due to profound defects in ciliogenesis and complete loss of mucociliary clearance. Organotypic airway cultures pinpoint TAp73 as necessary and sufficient for basal body docking, axonemal extension, and motility during the differentiation of MCC progenitors. Mechanistically, cross-species genomic analyses and complete ciliary rescue of knockout MCCs identify TAp73 as the conserved central transcriptional integrator of multiciliogenesis. TAp73 directly activates the key regulators FoxJ1, Rfx2, Rfx3, and miR34bc plus nearly 50 structural and functional ciliary genes, some of which are associated with human ciliopathies. Our results position TAp73 as a novel central regulator of MCC differentiation."],["dc.identifier.doi","10.1101/gad.279836.116"],["dc.identifier.isi","000378084000006"],["dc.identifier.pmid","27257214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40428"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cold Spring Harbor Lab Press, Publications Dept"],["dc.relation.issn","1549-5477"],["dc.relation.issn","0890-9369"],["dc.title","TAp73 is a central transcriptional regulator of airway multiciliogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]