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dc.contributor.authorDohi, Takehiko
dc.contributor.authorSalz, Whitney
dc.contributor.authorCosta, Marco R.
dc.contributor.authorAriyan, Charlotte
dc.contributor.authorBasadonna, Giacomo P.
dc.contributor.authorAltieri, Dario C.
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:50Z
dc.date.available2022-08-23T16:52:50Z
dc.date.issued2006-02-14
dc.date.submitted2008-07-09
dc.identifier.citation<p>EMBO Rep. 2006 Apr;7(4):438-43. Epub 2006 Feb 10. <a href="http://dx.doi.org/10.1038/sj.embor.7400640">Link to article on publisher's site</a></p>
dc.identifier.issn1469-221X (Print)
dc.identifier.doi10.1038/sj.embor.7400640
dc.identifier.pmid16470228
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42133
dc.description.abstractSurvivin is a cancer gene implicated in inhibition of apoptosis and regulation of mitosis, but its function in normal cells has remained elusive. Here, we show that transgenic mice expressing survivin in pancreatic islet beta-cells show no changes in cell proliferation, as determined by islet size or islet number. Transplantation of survivin transgenic islets in diabetic recipient mice affords long-term engraftment and stable correction of hyperglycaemia. This involves intrinsic inhibition of beta-cell apoptosis, in vivo, and global transcriptional changes in pancreatic islets with upregulation of stress response genes, antagonists of cytokine signalling and promoters of angiogenesis. These broad cytoprotective functions of survivin in vivo might be beneficial for gene therapy of diabetes.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16470228&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456913/
dc.subjectAnimals
dc.subject*Apoptosis
dc.subjectCell Line
dc.subjectDiabetes Mellitus
dc.subjectGene Expression Regulation
dc.subjectHumans
dc.subjectIslets of Langerhans
dc.subject*Islets of Langerhans Transplantation
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Transgenic
dc.subjectMicrotubule-Associated Proteins
dc.subjectNeoplasm Proteins
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleInhibition of apoptosis by survivin improves transplantation of pancreatic islets for treatment of diabetes in mice
dc.typeJournal Article
dc.source.journaltitleEMBO reports
dc.source.volume7
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/508
dc.identifier.contextkey544990
html.description.abstract<p>Survivin is a cancer gene implicated in inhibition of apoptosis and regulation of mitosis, but its function in normal cells has remained elusive. Here, we show that transgenic mice expressing survivin in pancreatic islet beta-cells show no changes in cell proliferation, as determined by islet size or islet number. Transplantation of survivin transgenic islets in diabetic recipient mice affords long-term engraftment and stable correction of hyperglycaemia. This involves intrinsic inhibition of beta-cell apoptosis, in vivo, and global transcriptional changes in pancreatic islets with upregulation of stress response genes, antagonists of cytokine signalling and promoters of angiogenesis. These broad cytoprotective functions of survivin in vivo might be beneficial for gene therapy of diabetes.</p>
dc.identifier.submissionpathoapubs/508
dc.contributor.departmentDepartment of Surgery
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages438-43


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