Mansouri, Ahmed

[["dc.bibliographiccitation.firstpage","3948"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3957"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Shamsi, Farnaz"],["dc.contributor.author","Parlato, Rosanna"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T09:31:14Z"],["dc.date.available","2018-11-07T09:31:14Z"],["dc.date.issued","2014"],["dc.description.abstract","The putative induction of adult -cell regeneration represents a promising approach for the treatment of type 1 diabetes. Toward this ultimate goal, it is essential to develop an inducible model mimicking the long-lasting disease progression. In the current study, we have established a novel -cell ablation mouse model, in which the -cell mass progressively declines, as seen in type 1 diabetes. The model is based on the -cell specific genetic ablation of the transcription initiation factor 1A, TIF-IA, essential for RNA Polymerase I activity (TIF-IA(/)). Using this approach, we induced a slow apoptotic response that eventually leads to a protracted -cell death. In this model, we observed -cell regeneration that resulted in a complete recovery of the -cell mass and normoglycemia. In addition, we showed that adaptive proliferation of remaining -cells is the prominent mechanism acting to compensate for the massive -cell loss in young but also aged mice. Interestingly, at any age, we also detected -like cells expressing the glucagon hormone, suggesting a transition between - and -cell identities or vice versa. Taken together, the TIF-IA(/) mouse model can be used to investigate the potential therapeutic approaches for type 1 diabetes targeting -cell regeneration."],["dc.identifier.doi","10.4161/15384101.2014.952176"],["dc.identifier.isi","000348329600024"],["dc.identifier.pmid","25558832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31496"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1551-4005"],["dc.relation.issn","1538-4101"],["dc.title","A genetic mouse model for progressive ablation and regeneration of insulin producing beta-cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.issue","1"],["dc.bibliographiccitation.journal","Tissue Antigens"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hamann, Carina"],["dc.contributor.author","Elsner, Leslie"],["dc.contributor.author","Nolte, Jessica"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Guan, Kaomei"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Dressel, Ralf"],["dc.date.accessioned","2018-11-07T09:38:32Z"],["dc.date.available","2018-11-07T09:38:32Z"],["dc.date.issued","2014"],["dc.format.extent","5"],["dc.identifier.isi","000337546000002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33083"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.eventlocation","Stockholm, SWEDEN"],["dc.relation.issn","1399-0039"],["dc.relation.issn","0001-2815"],["dc.title","PLURIPOTENT STEM CELLS VARYING IN A SINGLE MINOR HISTOCOMPATIBILITY ANTIGEN ELICIT CELLULAR AND HUMORAL IMMUNE RESPONSES THAT CAN MEDIATE GRAFT REJECTION"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","103787"],["dc.bibliographiccitation.journal","Ore Geology Reviews"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Alibabaie, N."],["dc.contributor.author","Esmaeily, D."],["dc.contributor.author","Peters, S.T.M."],["dc.contributor.author","Horn, I."],["dc.contributor.author","Gerdes., A."],["dc.contributor.author","Nirooamand, S."],["dc.contributor.author","Jian, W."],["dc.contributor.author","Mansouri, T."],["dc.contributor.author","Tudeshki, H."],["dc.contributor.author","Lehmann, B."],["dc.date.accessioned","2021-04-14T08:28:41Z"],["dc.date.available","2021-04-14T08:28:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.oregeorev.2020.103787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82683"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0169-1368"],["dc.title","Evolution of the Kiruna-type Gol-e-Gohar iron ore district, Sanandaj-Sirjan zone, Iran"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Developmental Cell"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Al-Hasani, Keith"],["dc.contributor.author","Pfeifer, Anja"],["dc.contributor.author","Courtney, Monica"],["dc.contributor.author","Ben-Othman, Nouha"],["dc.contributor.author","Gjernes, Elisabet"],["dc.contributor.author","Vieira, Andhira"],["dc.contributor.author","Druelle, Noemie"],["dc.contributor.author","Avolio, Fabio"],["dc.contributor.author","Ravassard, Philippe"],["dc.contributor.author","Leuckx, Gunter"],["dc.contributor.author","Lacas-Gervais, Sandra"],["dc.contributor.author","Ambrosetti, Damien"],["dc.contributor.author","Benizri, Emmanuel"],["dc.contributor.author","Hecksher-Sorensen, Jacob"],["dc.contributor.author","Gounon, Pierre"],["dc.contributor.author","Ferrer, Jorge"],["dc.contributor.author","Gradwohl, Gerard"],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Collombat, Patrick"],["dc.date.accessioned","2018-11-07T09:22:22Z"],["dc.date.available","2018-11-07T09:22:22Z"],["dc.date.issued","2013"],["dc.description.abstract","It was recently demonstrated that embryonic glucagon-producing cells in the pancreas can regenerate and convert into insulin-producing beta-like cells through the constitutive/ectopic expression of the Pax4 gene. However, whether alpha cells in adult mice display the same plasticity is unknown. Similarly, the mechanisms underlying such reprogramming remain unclear. We now demonstrate that the misexpression of Pax4 in glucagon(+) cells age-independently induces their conversion into beta-like cells and their glucagon shortage-mediated replacement, resulting in islet hypertrophy and in an unexpected islet neogenesis. Combining several lineage-tracing approaches, we show that, upon Pax4-mediated alpha-to-beta-like cell conversion, pancreatic duct-lining precursor cells are continuously mobilized, re-express the developmental gene Ngn3, and successively adopt a glucagon+ and a beta-like cell identity through a mechanism involving the reawakening of the epithelial-to-mesenchymal transition. Importantly, these processes can repeatedly regenerate the whole beta cell mass and thereby reverse several rounds of toxin-induced diabetes, providing perspectives to design therapeutic regenerative strategies."],["dc.identifier.doi","10.1016/j.devcel.2013.05.018"],["dc.identifier.isi","000322087400009"],["dc.identifier.pmid","23810513"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29326"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1534-5807"],["dc.title","Adult Duct-Lining Cells Can Reprogram into beta-like Cells Able to Counter Repeated Cycles of Toxin-Induced Diabetes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","838"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Seminars in Cell and Developmental Biology"],["dc.bibliographiccitation.lastpage","844"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Collombat, Patrick"],["dc.contributor.author","Xu, X."],["dc.contributor.author","Heimberg, Harry"],["dc.contributor.author","Mansouri, Ahmed"],["dc.date.accessioned","2018-11-07T08:38:58Z"],["dc.date.available","2018-11-07T08:38:58Z"],["dc.date.issued","2010"],["dc.description.abstract","The pancreas is composed of two main compartments consisting of endocrine and exocrine tissues. The majority of the organ is exocrine and responsible for the synthesis of digestive enzymes and for their transport via an intricate ductal system into the duodenum. The endocrine tissue represents less than 2% of the organ and is organized into functional units called islets of Langerhans, comprising alpha-, beta-, delta-, epsilon- and PP-cells, producing the hormones glucagon, insulin, somatostatin, ghrelin and pancreatic polypeptide (PP), respectively. Insulin-producing beta- cells play a central role in the control of the glucose homeostasis. Accordingly, absolute or relative deficiency in beta-cells may ultimately lead to type 1 and/or type 2 diabetes, respectively. One major goal of diabetes research is therefore to understand the molecular mechanisms controlling the development of beta-cells during pancreas morphogenesis, but also those underlying the regeneration of adult injured pancreas, and assess their significance for future cell-based therapy. In this review, we will therefore present new insights into beta-cell development with focus on beta-cell regeneration. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.semcdb.2010.07.007"],["dc.identifier.isi","000283598400010"],["dc.identifier.pmid","20688184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18878"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1084-9521"],["dc.title","Pancreatic beta-cells: From generation to regeneration"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]