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- aggregation classification "A1".
- aggregation creator B584047.
- aggregation creator B584048.
- aggregation creator B584049.
- aggregation creator B584050.
- aggregation creator B584051.
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- aggregation creator person.
- aggregation date "2010".
- aggregation format "application/pdf".
- aggregation hasFormat 1235510.bibtex.
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- aggregation hasFormat 1235510.yaml.
- aggregation isPartOf urn:issn:0012-1797.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Medicine and Health Sciences".
- aggregation title "Ectopic expression of E2F1 stimulates beta-Cell proliferation and function".
- aggregation abstract "OBJECTIVE-Generating functional beta-cells by inducing their proliferation may provide new perspectives for cell therapy in diabetes. Transcription factor E2F1 controls G(1)- to S-phase transition during the cycling of many cell types and is required for pancreatic beta-cell growth and function. However, the consequences of overexpression of E2F1 in beta-cells are unknown. RESEARCH DESIGN AND METHODS-The effects of E2F1 overexpression on beta-cell proliferation and function were analyzed in isolated rat beta-cells and in transgenic mice. RESULTS-Adenovirus AdE2F1-mediated overexpression of E2F1 increased the proliferation of isolated primary rat beta-cells 20-fold but also enhanced beta-cell death. Coinfection with adenovirus Ad Akt expressing a constitutively active form of Akt (protein kinase B) suppressed beta-cell death to control levels. At 48 h after infection, the total beta-cell number and insulin content were, respectively, 46 and 79% higher in AdE2F1+AdAkt-infected cultures compared with untreated. Conditional overexpression of E2F1 in mice resulted in a twofold increase of beta-cell proliferation and a 70% increase of pancreatic insulin content, but did not increase beta-cell mass. Glucose-challenged insulin release was increased, and the mice showed protection against toxin-induced diabetes. CONCLUSIONS-Overexpression of E2F1, either in vitro or in vivo, can stimulate beta-cell proliferation activity. In vivo E2F1 expression significantly increases the insulin content and function of adult beta-cells, making it a strategic target for therapeutic manipulation of beta-cell function. Diabetes 59:1435-1444, 2010".
- aggregation authorList BK937142.
- aggregation endPage "1444".
- aggregation issue "6".
- aggregation startPage "1435".
- aggregation volume "59".
- aggregation aggregates 1256364.
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