JCI table of contents, 1...( cluded that these two members have dist...)

cluded that these two members have distinct roles in T lymphocyte homeostasis. They now show that E2F1 an E2F2 are critical for proper pancreatic development and function, as mice deficient in both these genes develop diabetes and exocrine gland dysfunction. Loss of both these factors results in gross abnormalities in pancreatic function as the mice age, and disease manifests as diabetes due to lack of insulin. Cell cycle assays showed increased proliferation and apoptosis in the double-knockout mouse cells. These results suggest the involvement of E2F1 and E2F2 in the maintenance of differentiated cells in the pancreas and support their distinct role as transcriptional repressors that cannot be compensated for by other members of the gene family.

TITLE: Diabetes and exocrine pancreatic insufficiency in E2F1/E2F2 double-mutant mice

AUTHOR CONTACT:
Ana Zubiaga
University of the Basque Country, Bilbao, Spain.
Phone: 34-94-601-2603; Fax: 34-94-464-8500; E-mail: ggpzuela@lg.ehu.es

View the PDF of this article at: https://www.the-jci.org/press/18879.pdf

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CD39 Thins Out Thrombosis

Vascular thrombosis results from platelet recruitment and aggregation at a site of vascular injury. CD39 converts ATP and ADP to AMP, which can be further degraded to adenosine, an antithrombotic mediator. Anthony d'Apice and colleagues, from St. Vincent's Hospital, Melbourne, pursued CD39 as a potential antithrombosis agent in disease and in transplantation using mice transgenic for human CD39. hCD39-transgenic mice had increased bleeding times and were also protected from collagen-induced thrombosis. Moreover, the study showed that hCD39 expression in either endothelial cells alone or blood components alone was sufficient to increase bleeding times. To test CD39's potential in imp
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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
17-May-2004

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