Mansouri, Ahmed

[["dc.bibliographiccitation.firstpage","37906"],["dc.bibliographiccitation.issue","35"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","37918"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Kosinsky, Robyn L."],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Hellbach, Nicole"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Vogel, Tanja"],["dc.contributor.author","Begus-Nahrmann, Yvonne"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2019-07-09T11:42:03Z"],["dc.date.available","2019-07-09T11:42:03Z"],["dc.date.issued","2015-11-10"],["dc.description.abstract","Epigenetic regulatory mechanisms play a central role in controlling gene expression during development, cell differentiation and tumorigenesis. Monoubiquitination of histone H2B is one epigenetic modification which is dynamically regulated by the opposing activities of specific ubiquitin ligases and deubiquitinating enzymes (DUBs). The Ubiquitin-specific Protease 22 (USP22) is the ubiquitin hydrolase component of the human SAGA complex which deubiquitinates histone H2B during transcription. Recently, many studies have investigated an oncogenic potential of USP22 overexpression. However, its physiological function in organ maintenance, development and its cellular function remain largely unknown. A previous study reported embryonic lethality in Usp22 knockout mice. Here we describe a mouse model with a global reduction of USP22 levels which expresses the LacZ gene under the control of the endogenous Usp22 promoter. Using this reporter we found Usp22 to be ubiquitously expressed in murine embryos. Notably, adult Usp22lacZ/lacZ displayed low residual Usp22 expression levels coupled with a reduced body size and weight. Interestingly, the reduction of Usp22 significantly influenced the frequency of differentiated cells in the small intestine and the brain while H2B and H2Bub1 levels remained constant. Taken together, we provide evidence for a physiological role for USP22 in controlling cell differentiation and lineage specification."],["dc.identifier.doi","10.18632/oncotarget.5412"],["dc.identifier.pmid","26431380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12736"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58576"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Usp22 deficiency impairs intestinal epithelial lineage specification in vivo."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","640956"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","ISRN Endocrinology"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","2012"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2019-07-09T11:55:02Z"],["dc.date.available","2019-07-09T11:55:02Z"],["dc.date.issued","2012"],["dc.description.abstract","The pancreas is composed of two compartments that deliver digestive enzymes and endocrine hormones to control the blood sugar level. The endocrine pancreas consists of functional units organized into cell clusters called islets of Langerhans where insulinproducing cells are found in the core and surrounded by glucagon-, somatostatin-, pancreatic polypeptide-, and ghrelin-producing cells. Diabetes is a devastating disease provoked by the depletion or malfunction of insulin-producing beta-cells in the endocrine pancreas. The side effects of diabetes are multiple, including cardiovascular, neuropathological, and kidney diseases. The analyses of transgenic and knockout mice gave major insights into the molecular mechanisms controlling endocrine pancreas genesis. Moreover, the study of animal models of pancreas injury revealed that the pancreas has the propensity to undergo regeneration and opened new avenues to develop novel therapeutic approaches for the treatment of diabetes. Thus, beside self-replication of preexisting insulin-producing cells, several potential cell sources in the adult pancreas were suggested to contribute to beta-cell regeneration, including acinar, intraislet, and duct epithelia. However, regeneration in the adult endocrine pancreas is still under controversial debate."],["dc.format.extent","13"],["dc.identifier.doi","10.5402/2012/640956"],["dc.identifier.fs","591334"],["dc.identifier.pmid","23326678"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60782"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-4649"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0/"],["dc.title","Development and Regeneration in the Endocrine Pancreas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1004468"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Haro, Endika"],["dc.contributor.author","Delgado, Irene"],["dc.contributor.author","Junco, Marisa"],["dc.contributor.author","Yamada, Yoshihiko"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Oberg, Kerby C."],["dc.contributor.author","Ros, Marian A."],["dc.date.accessioned","2018-11-07T09:36:56Z"],["dc.date.available","2018-11-07T09:36:56Z"],["dc.date.issued","2014"],["dc.description.abstract","The formation and maintenance of the apical ectodermal ridge (AER) is critical for the outgrowth and patterning of the vertebrate limb. The induction of the AER is a complex process that relies on integrated interactions among the Fgf, Wnt, and Bmp signaling pathways that operate within the ectoderm and between the ectoderm and the mesoderm of the early limb bud. The transcription factors Sp6 and Sp8 are expressed in the limb ectoderm and AER during limb development. Sp6 mutant mice display a mild syndactyly phenotype while Sp8 mutants exhibit severe limb truncations. Both mutants show defects in AER maturation and in dorsal-ventral patterning. To gain further insights into the role Sp6 and Sp8 play in limb development, we have produced mice lacking both Sp6 and Sp8 activity in the limb ectoderm. Remarkably, the elimination or significant reduction in Sp6; Sp8 gene dosage leads to tetra-amelia; initial budding occurs, but neither Fgf8 nor En1 are activated. Mutants bearing a single functional allele of Sp8 (Sp6(-/-); Sp8(+/-)) exhibit a split-hand/foot malformation phenotype with double dorsal digit tips probably due to an irregular and immature AER that is not maintained in the center of the bud and on the abnormal expansion of Wnt7a expression to the ventral ectoderm. Our data are compatible with Sp6 and Sp8 working together and in a dose-dependent manner as indispensable mediators of Wnt/catenin and Bmp signaling in the limb ectoderm. We suggest that the function of these factors links proximal-distal and dorsal-ventral patterning."],["dc.identifier.doi","10.1371/journal.pgen.1004468"],["dc.identifier.isi","000341577800003"],["dc.identifier.pmid","25166858"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10862"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32726"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.relation.issn","1553-7390"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Sp6 and Sp8 Transcription Factors Control AER Formation and Dorsal-Ventral Patterning in Limb Development"],["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","3243"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3244"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Al-Hasani, Keith"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Faurite, Biljana"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:18:37Z"],["dc.date.available","2018-11-07T09:18:37Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.4161/cc.26357"],["dc.identifier.isi","000327381100004"],["dc.identifier.pmid","24036539"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28443"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Induction of multiple cycles of pancreatic beta-cell replacement"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2622"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Schindehuette, Jan"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Novota, Peter"],["dc.contributor.author","Baier, Paul Christian"],["dc.contributor.author","Schillert, Arne"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Herrmann, Thomas R."],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T11:13:02Z"],["dc.date.available","2018-11-07T11:13:02Z"],["dc.date.issued","2008"],["dc.description.abstract","Embryonic stem (ES) cells have the potential to differentiate into all cell types and are considered as a valuable source of cells for transplantation therapies. A critical issue, however, is the risk of teratoma formation after transplantation. The effect of the immune response on the tumorigenicity of transplanted cells is poorly understood. We have systematically compared the tumorigenicity of mouse ES cells and in vitro differentiated neuronal cells in various recipients. Subcutaneous injection of 1 x 10(6) ES or differentiated cells into syngeneic or allogeneic immunodeficient mice resulted in teratomas in about 95% of the recipients. Both cell types did not give rise to tumors in immunocompetent allogeneic mice or xenogeneic rats. However, in 61% of cyclosporine A-treated rats teratomas developed after injection of differentiated cells. Undifferentiated ES cells did not give rise to tumors in these rats. ES cells turned out to be highly susceptible to killing by rat natural killer (NK) cells due to the expression of ligands of the activating NK receptor NKG2D on ES cells. These ligands were downregulated on differentiated cells. The activity of NK cells which is not suppressed by cyclosporine A might contribute to the prevention of teratomas after injection of ES cells but not after inoculation of differentiated cells. These findings clearly point to the importance of the immune response in this process. Interestingly, the differentiated cells must contain a tumorigenic cell population that is not present among ES cells and which might be resistant to NK cell-mediated killing."],["dc.identifier.doi","10.1371/journal.pone.0002622"],["dc.identifier.isi","000264065800024"],["dc.identifier.pmid","18612432"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53801"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Tumorigenicity of Mouse Embryonic Stem Cells and In Vitro Differentiated Neuronal Cells Is Controlled by the Recipients' Immune Response"],["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.artnumber","e1003934"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Ravaud, Christophe"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Leuckx, Gunter"],["dc.contributor.author","Lacas-Gervais, Sandra"],["dc.contributor.author","Burel-Vandenbos, Fanny"],["dc.contributor.author","Ambrosetti, Damien"],["dc.contributor.author","Hecksher-Sorensen, Jacob"],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:18:47Z"],["dc.date.available","2018-11-07T09:18:47Z"],["dc.date.issued","2013"],["dc.description.abstract","Recently, it was demonstrated that pancreatic new-born glucagon-producing cells can regenerate and convert into insulinproducing beta-like cells through the ectopic expression of a single gene, Pax4. Here, combining conditional loss-of-function and lineage tracing approaches, we show that the selective inhibition of the Arx gene in alpha-cells is sufficient to promote the conversion of adult alpha-cells into beta-like cells at any age. Interestingly, this conversion induces the continuous mobilization of duct-lining precursor cells to adopt an endocrine cell fate, the glucagon(+) cells thereby generated being subsequently converted into beta-like cells upon Arx inhibition. Of interest, through the generation and analysis of Arx and Pax4 conditional double-mutants, we provide evidence that Pax4 is dispensable for these regeneration processes, indicating that Arx represents the main trigger of alpha-cell-mediated beta-like cell neogenesis. Importantly, the loss of Arx in alpha-cells is sufficient to regenerate a functional beta-cell mass and thereby reverse diabetes following toxin-induced beta-cell depletion. Our data therefore suggest that strategies aiming at inhibiting the expression of Arx, or its molecular targets/co-factors, may pave new avenues for the treatment of diabetes."],["dc.identifier.doi","10.1371/journal.pgen.1003934"],["dc.identifier.isi","000330367200085"],["dc.identifier.pmid","24204325"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9441"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28484"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Inactivation of Arx in Pancreatic alpha-Cells Triggers Their Neogenesis and Conversion into Functional beta-Like Cells"],["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.artnumber","e1006274"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS Genetics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bachmann, Christina"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Rabe, Tamara I."],["dc.contributor.author","Patwa, Megha"],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Ashery-Padan, Ruth"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2018-11-07T10:09:05Z"],["dc.date.available","2018-11-07T10:09:05Z"],["dc.date.issued","2016"],["dc.description.abstract","Neurogenesis is a key developmental event through which neurons are generated from neural stem/progenitor cells. Chromatin remodeling BAF (mSWI/SNF) complexes have been reported to play essential roles in the neurogenesis of the central nervous system. However, whether BAF complexes are required for neuron generation in the olfactory system is unknown. Here, we identified onscBAF and ornBAF complexes, which are specifically present in olfactory neural stem cells (oNSCs) and olfactory receptor neurons (ORNs), respectively. We demonstrated that BAF155 subunit is highly expressed in both oNSCs and ORNs, whereas high expression of BAF170 subunit is observed only in ORNs. We report that conditional deletion of BAF155, a core subunit in both onscBAF and ornBAF complexes, causes impaired proliferation of oNSCs as well as defective maturation and axonogenesis of ORNs in the developing olfactory epithelium (OE), while the high expression of BAF170 is important for maturation of ORNs. Interestingly, in the absence of BAF complexes in BAF155/BAF170 double-conditional knockout mice (dcKO), OE is not specified. Mechanistically, BAF complex is required for normal activation of Pax6-dependent transcriptional activity in stem cells/progenitors of the OE. Our findings unveil a novel mechanism mediated by the mSWI/SNF complex in OE neurogenesis and development."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pgen.1006274"],["dc.identifier.isi","000386069000012"],["dc.identifier.pmid","27611684"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39592"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1553-7404"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","mSWI/SNF (BAF) Complexes Are Indispensable for the Neurogenesis and Development of Embryonic Olfactory Epithelium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0201536"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Vergoni, Bastien"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Druelle, Noémie"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Hadzic, Biljana"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Napolitano, Tiziana"],["dc.contributor.author","Navarro Sanz, Sergi"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.editor","Rooman, Ilse"],["dc.date.accessioned","2020-12-10T18:42:07Z"],["dc.date.available","2020-12-10T18:42:07Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1371/journal.pone.0201536"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77817"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Neurog3 misexpression unravels mouse pancreatic ductal cell plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","39"],["dc.bibliographiccitation.journal","Neural Development"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Rabe, Tamara I."],["dc.contributor.author","Griesel, Gundula"],["dc.contributor.author","Blanke, Stephen"],["dc.contributor.author","Kispert, Andreas"],["dc.contributor.author","Leitges, Michael"],["dc.contributor.author","van der Zwaag, Bert"],["dc.contributor.author","Burbach, J. Peter H."],["dc.contributor.author","Varoqueaux, Frederique"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:02:22Z"],["dc.date.available","2018-11-07T09:02:22Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: The homeobox containing transcription factor Uncx4.1 is, amongst others, expressed in the mouse midbrain. The early expression of this transcription factor in the mouse, as well as in the chick midbrain, points to a conserved function of Uncx4.1, but so far a functional analysis in this brain territory is missing. The goal of the current study was to analyze in which midbrain neuronal subgroups Uncx4.1 is expressed and to examine whether this factor plays a role in the early development of these neuronal subgroups. Results: We have shown that Uncx4.1 is expressed in GABAergic, glutamatergic and dopaminergic neurons in the mouse midbrain. In midbrain dopaminergic (mDA) neurons Uncx4.1 expression is particularly high around E11.5 and strongly diminished already at E17.5. The analysis of knockout mice revealed that the loss of Uncx4.1 is accompanied with a 25% decrease in the population of mDA neurons, as marked by tyrosine hydroxylase (TH), dopamine transporter (DAT), Pitx3 and Ngn2. In contrast, the number of glutamatergic Pax6-positive cells was augmented, while the GABAergic neuron population appears not affected in Uncx4.1-deficient embryos. Conclusion: We conclude that Uncx4.1 is implicated in the development of mDA neurons where it displays a unique temporal expression profile in the early postmitotic stage. Our data indicate that the mechanism underlying the role of Uncx4.1 in mDA development is likely related to differentiation processes in postmitotic stages, and where Ngn2 is engaged. Moreover, Uncx4.1 might play an important role during glutamatergic neuronal differentiation in the mouse midbrain."],["dc.identifier.doi","10.1186/1749-8104-7-39"],["dc.identifier.isi","000315088300001"],["dc.identifier.pmid","23217170"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24669"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1749-8104"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","The transcription factor Uncx4.1 acts in a short window of midbrain dopaminergic neuron differentiation"],["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.artnumber","32"],["dc.bibliographiccitation.journal","Genome Biology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Xie, Wanhua"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Indenbirken, Daniela"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:27:18Z"],["dc.date.available","2018-11-07T10:27:18Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Monoubiquitination of H2B (H2Bub1) is a largely enigmatic histone modification that has been linked to transcriptional elongation. Because of this association, it has been commonly assumed that H2Bub1 is an exclusively positively acting histone modification and that increased H2Bub1 occupancy correlates with increased gene expression. In contrast, depletion of the H2B ubiquitin ligases RNF20 or RNF40 alters the expression of only a subset of genes. Results: Using conditional Rnf40 knockout mouse embryo fibroblasts, we show that genes occupied by low to moderate amounts of H2Bub1 are selectively regulated in response to Rnf40 deletion, whereas genes marked by high levels of H2Bub1 are mostly unaffected by Rnf40 loss. Furthermore, we find that decreased expression of RNF40-dependent genes is highly associated with widespread narrowing of H3K4me3 peaks. H2Bub1 promotes the broadening of H3K4me3 to increase transcriptional elongation, which together lead to increased tissue- specific gene transcription. Notably, genes upregulated following Rnf40 deletion, including Foxl2, are enriched for H3K27me3, which is decreased following Rnf40 deletion due to decreased expression of the Ezh2 gene. As a consequence, increased expression of some RNF40-\"suppressed\" genes is associated with enhancer activation via FOXL2. Conclusion: Together these findings reveal the complexity and context-dependency whereby one histone modification can have divergent effects on gene transcription. Furthermore, we show that these effects are dependent upon the activity of other epigenetic regulatory proteins and histone modifications."],["dc.identifier.doi","10.1186/s13059-017-1159-5"],["dc.identifier.isi","000394828000003"],["dc.identifier.pmid","28209164"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14250"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43221"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/14993 but duplicate"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1474-760X"],["dc.rights","CC BY 4.0"],["dc.rights.access","openAccess"],["dc.rights.holder","The Author(s)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","RNF40 regulates gene expression in an epigenetic context-dependent manner"],["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"]]