Mansouri, Ahmed

[["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","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"]]

[["dc.bibliographiccitation.firstpage","248"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","World journal of stem cells"],["dc.bibliographiccitation.lastpage","255"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Liao, Mei-Chih"],["dc.contributor.author","Diaconu, Mihaela"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Timaeus, Charles"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Paulus, Walter"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2019-07-09T11:42:00Z"],["dc.date.available","2019-07-09T11:42:00Z"],["dc.date.issued","2014-04-26"],["dc.description.abstract","AIM: To find a safe source for dopaminergic neurons, we generated neural progenitor cell lines from human embryonic stem cells. METHODS: The human embryonic stem (hES) cell line H9 was used to generate human neural progenitor (HNP) cell lines. The resulting HNP cell lines were differentiated into dopaminergic neurons and analyzed by quantitative real-time polymerase chain reaction and immunofluorescence for the expression of neuronal differentiation markers, including beta-III tubulin (TUJ1) and tyrosine hydroxylase (TH). To assess the risk of teratoma or other tumor formation, HNP cell lines and mouse neuronal progenitor (MNP) cell lines were injected subcutaneously into immunodeficient SCID/beige mice. RESULTS: We developed a fairly simple and fast protocol to obtain HNP cell lines from hES cells. These cell lines, which can be stored in liquid nitrogen for several years, have the potential to differentiate in vitro into dopaminergic neurons. Following day 30 of differentiation culture, the majority of the cells analyzed expressed the neuronal marker TUJ1 and a high proportion of these cells were positive for TH, indicating differentiation into dopaminergic neurons. In contrast to H9 ES cells, the HNP cell lines did not form tumors in immunodeficient SCID/beige mice within 6 mo after subcutaneous injection. Similarly, no tumors developed after injection of MNP cells. Notably, mouse ES cells or neuronal cells directly differentiated from mouse ES cells formed teratomas in more than 90% of the recipients. CONCLUSION: Our findings indicate that neural progenitor cell lines can differentiate into dopaminergic neurons and bear no risk of generating teratomas or other tumors in immunodeficient mice."],["dc.identifier.doi","10.4252/wjsc.v6.i2.248"],["dc.identifier.fs","604380"],["dc.identifier.pmid","24772251"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12652"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58563"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1948-0210"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Embryonic stem cell-derived neural progenitors as non-tumorigenic source for dopaminergic neurons."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","52"],["dc.bibliographiccitation.journal","BMC Developmental Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Kordowich, Simon"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Serup, Palle"],["dc.date.accessioned","2018-11-07T08:53:03Z"],["dc.date.available","2018-11-07T08:53:03Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: Nkx2.2 and Arx represent key transcription factors implicated in the specification of islet cell subtypes during pancreas development. Mice deficient for Arx do not develop any alpha-cells whereas beta- and delta-cells are found in considerably higher numbers. In Nkx2.2 mutant animals, alpha- and beta-cell development is severely impaired whereas a ghrelin-expressing cell population is found augmented. Notably, Arx transcription is clearly enhanced in Nkx2.2-deficient pancreata. Hence in order to precise the functional link between both factors we performed a comparative analysis of Nkx2.2/Arx single- and double-mutants but also of Pax6-deficient animals. Results: We show that most of the ghrelin(+) cells emerging in pancreata of Nkx2.2- and Pax6-deficient mice, express the alpha-cell specifier Arx, but also additional beta-cell related genes. In Nkx2.2-deficient mice, Arx directly co-localizes with iAPP, PC1/3 and Pdx1 suggesting an Nkx2.2-dependent control of Arx in committed beta-cells. The combined loss of Nkx2.2 and Arx likewise results in the formation of a hyperplastic ghrelin(+) cell population at the expense of mature alpha- and beta-cells. Surprisingly, such Nkx2.2(-/-)Arx(-) ghrelin(+) cells also express the somatostatin hormone. Conclusions: Our data indicate that Nkx2.2 acts by reinforcing the transcriptional networks initiated by Pax4 and Arx in early committed beta- and alpha-cell, respectively. Our analysis also suggests that one of the coupled functions of Nkx2.2 and Pax4 is to counteract Arx gene activity in early committed beta-cells."],["dc.identifier.doi","10.1186/1471-213X-11-52"],["dc.identifier.isi","000295264200001"],["dc.identifier.pmid","21880149"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6945"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22316"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-213X"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Arx and Nkx2.2 compound deficiency redirects pancreatic alpha- and beta-cell differentiation to a somatostatin/ghrelin co-expressing cell lineage"],["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","1215"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Transgenic Research"],["dc.bibliographiccitation.lastpage","1220"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Kordowich, Simon"],["dc.contributor.author","Serup, Palle"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:03:01Z"],["dc.date.available","2018-11-07T09:03:01Z"],["dc.date.issued","2012"],["dc.description.abstract","Pax4 belongs to the paired-box family of transcription factors. The analysis of loss- and gain-of-function mutant animals revealed that this factor plays a crucial role in the endocrine pancreas. Indeed, Pax4 is required for the genesis of insulin-producing beta-cells. Remarkably, the sole misexpression of Pax4 in glucagon-expressing cells is able to induce their regeneration, endow these with beta-cell features, and thereby counter chemically induced diabetes. However, the function of Pax4 in adult endocrine cells remains unclear. Herein, we report the generation of Pax4 conditional knockout mice that will allow the analysis of Pax4 function in mature beta-cells, as well as in the adult central nervous system."],["dc.identifier.doi","10.1007/s11248-012-9624-0"],["dc.identifier.isi","000311496500006"],["dc.identifier.pmid","22717987"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8868"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24808"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0962-8819"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Generation of animals allowing the conditional inactivation of the Pax4 gene"],["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","e0144597"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ahmad, Zeeshan"],["dc.contributor.author","Rafeeq, Maria"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:47:33Z"],["dc.date.available","2018-11-07T09:47:33Z"],["dc.date.issued","2015"],["dc.description.abstract","The transcription factor Pax6 is an important regulator of development and cell differentiation in various organs. Thus, Pax6 was shown to promote neural development in the cerebral cortex and spinal cord, and to control pancreatic endocrine cell genesis. However, the role of Pax6 in distinct endocrine cells of the adult pancreas has not been addressed. We report the conditional inactivation of Pax6 in insulin and glucagon producing cells of the adult mouse pancreas. In the absence of Pax6, beta- and alpha-cells lose their molecular maturation characteristics. Our findings provide strong evidence that Pax6 is responsible for the maturation of beta-, and alpha-cells, but not of delta-, and PP-cells. Moreover, lineage-tracing experiments demonstrate that Pax6-deficient beta- and alpha-cells are shunted towards ghrelin marked cells, sustaining the idea that ghrelin may represent a marker for endocrine cell maturation."],["dc.identifier.doi","10.1371/journal.pone.0144597"],["dc.identifier.isi","000366903600062"],["dc.identifier.pmid","26658466"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12647"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35139"],["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 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Pax6 Inactivation in the Adult Pancreas Reveals Ghrelin as Endocrine Cell Maturation Marker"],["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"]]