Mansouri, Ahmed

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[["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.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"]]