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dc.contributor.authorPetrenko, Volodymyr
dc.contributor.authorStolovich-Rain, Miri
dc.contributor.authorVandereycken, Bart
dc.contributor.authorGiovannoni, Laurianne
dc.contributor.authorStorch, Kai-Florian
dc.contributor.authorDor, Yuval
dc.contributor.authorChera, Simona
dc.contributor.authorDibner, Charna
dc.date.accessioned2021-05-11T12:43:21Z
dc.date.available2021-05-11T12:43:21Z
dc.date.created2020-12-13T22:22:59Z
dc.date.issued2020
dc.PublishedGenes & Development. 2020, 34 (23-24), 1650-1665.
dc.identifier.issn0890-9369
dc.identifier.urihttps://hdl.handle.net/11250/2754946
dc.description.abstractCircadian clocks in pancreatic islets participate in the regulation of glucose homeostasis. Here we examined the role of these timekeepers in β-cell regeneration after the massive ablation of β cells by doxycycline-induced expression of diphtheria toxin A (DTA) in Insulin-rtTA/TET-DTA mice. Since we crossed reporter genes expressing α- and β-cell-specific fluorescent proteins into these mice, we could follow the fate of α- and β cells separately. As expected, DTA induction resulted in an acute hyperglycemia, which was accompanied by dramatic changes in gene expression in residual β cells. In contrast, only temporal alterations of gene expression were observed in α cells. Interestingly, β cells entered S phase preferentially during the nocturnal activity phase, indicating that the diurnal rhythm also plays a role in the orchestration of β-cell regeneration. Indeed, in arrhythmic Bmal1-deficient mice, which lack circadian clocks, no compensatory β-cell proliferation was observed, and the β-cell ablation led to aggravated hyperglycemia, hyperglucagonemia, and fatal diabetes.en_US
dc.language.isoengen_US
dc.publisherCSH Pressen_US
dc.rightsNavngivelse-Ikkekommersiell 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/deed.no*
dc.titleThe core clock transcription factor BMAL1 drives circadian β-cell proliferation during compensatory regeneration of the endocrine pancreasen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2020 The Authorsen_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2
dc.identifier.doi10.1101/gad.343137.120
dc.identifier.cristin1859258
dc.source.journalGenes & Developmenten_US
dc.source.4034
dc.source.1423-24
dc.source.pagenumber1650-1665en_US
dc.identifier.citationGenes & Development. 2020, 34: 1650-1665en_US
dc.source.volume34en_US


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Navngivelse-Ikkekommersiell 4.0 Internasjonal
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