Moll, Ute M.

[["dc.bibliographiccitation.firstpage","1776"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","1781"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Palacios, Gustavo"],["dc.contributor.author","Talos, Flaminia"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Moll, Ute M."],["dc.contributor.author","Petrenko, Oleksi"],["dc.date.accessioned","2018-11-07T11:13:57Z"],["dc.date.available","2018-11-07T11:13:57Z"],["dc.date.issued","2008"],["dc.description.abstract","To better understand the role of E2F1 in tumor formation, we analyzed spontaneous tumorigenesis in p53(-/-)E2F1(+/+) and p53(-/-)E2F1(-/-) mice. We show that the combined loss of p53 and E2F1 leads to an increased incidence of sarcomas and carcinomas compared to the loss of p53 alone. E2F1-deficient tumors show wide chromosomal variation, indicative of genomic instability. Consistent with this, p53(-/-)E2F1(-/-) primary fibroblasts have a reduced capacity to maintain genomic stability when exposed to S-phase inhibitors or genotoxic drugs. A major mechanism of E2F1's contribution to genomic integrity lies in mediating stabilization and engagement of the Rb protein."],["dc.description.sponsorship","NCI NIH HHS [R01 CA060664-13, R01 CA060664]"],["dc.identifier.doi","10.4161/cc.7.12.6030"],["dc.identifier.isi","000257249300013"],["dc.identifier.pmid","18583939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54017"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","E2F1 plays a direct role in Rb stabilization and p53-independent tumor suppression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","647"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Cell"],["dc.bibliographiccitation.lastpage","659"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Talos, Flaminia"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Flores, Elsa R."],["dc.contributor.author","Petrenko, Oleksi"],["dc.contributor.author","Moll, Ute M."],["dc.date.accessioned","2018-11-07T10:59:36Z"],["dc.date.available","2018-11-07T10:59:36Z"],["dc.date.issued","2007"],["dc.description.abstract","Previous studies showed that p53 plays a central role in G1 and DNA damage checkpoints, thus contributing to genomic stability. We show here that p73 also plays a role in genomic integrity but this mechanism is manifest only when p53 is lost. Isolated p73 loss in primary cells does not induce genomic instability. Instead, it results in impaired proliferation and premature senescence due to compensatory activation of p53. Combined loss of p73 and p53 rescues these defects, but at the expense of exacerbated genomic instability. This leads to rapid increase in polyploidy and aneuploidy, markedly exceeding that of p53 loss alone. Constitutive deregulation of cyclin-Cdk activities and excess failure of the G2/M DNA damage checkpoint appear to fuel increased ploidy abnormalities upon p53/p73 loss, while primary mitotic defects do not play a causal role. These data indicate that p73 is essential for suppressing polyploidy and aneuploidy when p53 is inactivated."],["dc.identifier.doi","10.1016/j.molcel.2007.06.036"],["dc.identifier.isi","000249050200015"],["dc.identifier.pmid","17707235"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50741"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-2765"],["dc.title","p73 suppresses polyploidy and aneuploidy in the absence of functional p53"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Cell"],["dc.bibliographiccitation.lastpage","83"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Wienken, Magdalena"],["dc.contributor.author","Dickmanns, Antje"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Kramer, Daniela"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Weiss, Miriam"],["dc.contributor.author","Karpiuk, Oleksandra"],["dc.contributor.author","Kassem, Moustapha"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Lozano, Guillermina"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Moll, Ute M."],["dc.contributor.author","Zhang, X."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.date.accessioned","2018-11-07T10:19:27Z"],["dc.date.available","2018-11-07T10:19:27Z"],["dc.date.issued","2016"],["dc.description.abstract","The MDM2 oncoprotein ubiquitinates and antagonizes p53 but may also carry out p53-independent functions. Here we report that MDM2 is required for the efficient generation of induced pluripotent stem cells (iPSCs) from murine embryonic fibroblasts, in the absence of p53. Similarly, MDM2 depletion in the context of p53 deficiency also promoted the differentiation of human mesenchymal stem cells and diminished clonogenic survival of cancer cells. Most of the MDM2-controlled genes also responded to the inactivation of the Polycomb Repressor Complex 2 (PRC2) and its catalytic component EZH2. MDM2 physically associated with EZH2 on chromatin, enhancing the trimethylation of histone 3 at lysine 27 and the ubiquitination of histone 2A at lysine 119 (H2AK119) at its target genes. Removing MDM2 simultaneously with the H2AK119 E3 ligase Ring1B/RNF2 further induced these genes and synthetically arrested cell proliferation. In conclusion, MDM2 supports the Polycomb-mediated repression of lineage-specific genes, independent of p53."],["dc.identifier.doi","10.1016/j.molcel.2015.12.008"],["dc.identifier.isi","000372324500007"],["dc.identifier.pmid","26748827"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41663"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4164"],["dc.relation.issn","1097-2765"],["dc.title","MDM2 Associates with Polycomb Repressor Complex 2 and Enhances Stemness-Promoting Chromatin Modifications Independent of p53"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2070"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","2080"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Petrenko, Oleksi"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Palacios, Gustavo"],["dc.contributor.author","Moll, Ute M."],["dc.date.accessioned","2018-11-07T08:42:48Z"],["dc.date.available","2018-11-07T08:42:48Z"],["dc.date.issued","2010"],["dc.description.abstract","Mice engineered to express c-Myc in B cells (E mu-myc mice) develop lethal lymphomas in which the gene encoding the p53 tumor suppressor is frequently mutated. Whether the p53 homolog p73 also functions as a tumor suppressor in vivo remains controversial. Here we have shown that p73 loss does not substantially affect disease onset and mortality in E mu-myc mice. However, it does alter the phenotype of the disease. Specifically, p73 loss decreased nodal disease and increased widespread extranocial dissemination. We further found that p53 acted as the dominant tumor suppressor during the onset of E mu-myc-driven B cell lymphomagenesis, while p73 modulated tumor dissemination and extranodal growth. Immunophenotyping and expression profiling suggested that p73 loss allowed increased maturation of malignant B cells and deregulated genes involved in lymphocyte homing and dissemination of human lymphomas. Consistent with this, p73 expression was frequently downregulated in a large cohort of human mature aggressive B cell lymphomas, and both the incidence and degree of p73 downregulation in these tumors correlated with their extranodal dissemination status. These data indicate that p73 is a modifier of Myc-driven lymphomas in mice, favoring tumor dissemination, and suggest that p73 could be a biomarker for human B cell lymphoma dissemination, a notion that can now be tested in clinicopathologic correlation studies."],["dc.identifier.doi","10.1172/JCI40331"],["dc.identifier.isi","000278324400030"],["dc.identifier.pmid","20484818"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7565"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19786"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Investigation Inc"],["dc.relation.issn","0021-9738"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Loss of p73 promotes dissemination of Myc-induced B cell lymphomas in mice"],["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","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"]]

[["dc.bibliographiccitation.firstpage","1173"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","1190"],["dc.bibliographiccitation.volume","204"],["dc.contributor.author","Holembowski, Lena"],["dc.contributor.author","Kramer, Daniela"],["dc.contributor.author","Riedel, Dietmar"],["dc.contributor.author","Sordella, Raffaella"],["dc.contributor.author","Nemajerova, Alice"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Moll, Ute M."],["dc.date.accessioned","2018-11-07T09:42:22Z"],["dc.date.available","2018-11-07T09:42:22Z"],["dc.date.issued","2014"],["dc.description.abstract","A core evolutionary function of the p53 family is to protect the genomic integrity of gametes. However, the role of p73 in the male germ line is unknown. Here, we reveal that TAp73 unexpectedly functions as an adhesion and maturation factor of the seminiferous epithelium orchestrating spermiogenesis. TAp73 knockout (TAp73KO) and p73KO mice, but not. Np73KO mice, display a \"near-empty seminiferous tubule\" phenotype due to massive premature loss of immature germ cells. The cellular basis of this phenotype is defective cell-cell adhesions of developing germ cells to Sertoli nurse cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which leads to disruption of the adhesive integrity and maturation of the germ epithelium. At the molecular level, TAp73, which is produced in germ cells, controls a coordinated transcriptional program of adhesion-and migrationrelated proteins including peptidase inhibitors, proteases, receptors, and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuring. Thus, we propose the testis as a unique organ with strict division of labor among all family members: p63 and p53 safeguard germ line fidelity, whereas TAp73 ensures fertility by enabling sperm maturation."],["dc.description.sponsorship","National Cancer Institute [CA93853]; Deutsche Krebshilfe [108775]"],["dc.identifier.doi","10.1083/jcb.201306066"],["dc.identifier.isi","000333903600010"],["dc.identifier.pmid","24662569"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33940"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Rockefeller Univ Press"],["dc.relation.issn","1540-8140"],["dc.relation.issn","0021-9525"],["dc.title","TAp73 is essential for germ cell adhesion and maturation in testis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]