Lizé, Muriel

[["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","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","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.issue","5"],["dc.bibliographiccitation.journal","EJC SUPPLEMENTS"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Lize, M."],["dc.contributor.author","Herr, Christian"],["dc.contributor.author","Bals, R."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T08:42:32Z"],["dc.date.available","2018-11-07T08:42:32Z"],["dc.date.issued","2010"],["dc.identifier.isi","000288603100036"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19722"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","21st Meeting of the European-Association-for-Cancer-Research"],["dc.relation.eventlocation","Oslo, NORWAY"],["dc.title","miR-449 induces apoptosis while triggering a stress and DNA damage response"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Cancer"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Suazo, C. Gallinas"],["dc.contributor.author","Klimke, Alexander"],["dc.contributor.author","Lize, M."],["dc.contributor.author","Kessel, Michael"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T09:37:50Z"],["dc.date.available","2018-11-07T09:37:50Z"],["dc.date.issued","2014"],["dc.format.extent","S84"],["dc.identifier.isi","000351589700308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32930"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Sci Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","1879-0852"],["dc.relation.issn","0959-8049"],["dc.title","microRNA-449 acts as a barrier to stemness"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]