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Publication : E2F-1-induced p53-independent apoptosis in transgenic mice.

First Author  Holmberg C Year  1998
Journal  Oncogene Volume  17
Issue  2 Pages  143-55
PubMed ID  9674698 Mgi Jnum  J:89021
Mgi Id  MGI:3037615 Doi  10.1038/sj.onc.1201915
Citation  Holmberg C, et al. (1998) E2F-1-induced p53-independent apoptosis in transgenic mice. Oncogene 17(2):143-55
abstractText  The E2F transcription factors are key targets for the retinoblastoma protein, pRB. By inactivation of E2Fs, pRB prevents progression to the S phase. To test proliferative functions of E2F, we generated transgenic mice expressing human E2F-1 and/or human DP-1. When the hydroxymethyl glutaryl coenzyme A reductase promoter was used to express DP-1, overexpression occurred in a variety of tissues and did not confer phenotypic changes. In contrast, expression of E2F-1 from the same promoter was obtained only in testicles, in which E2F-1 overexpression caused atrophy and sterility through a process involving increased apoptosis in the germinal epithelium. This effect was potentiated by simultaneous overexpression of DP-1. Testicular atrophy as a result of overexpression of E2F-1 and DP-1 is independent of functional p53, since p53-nullizygous transgenic mice overexpressing E2F-1 and DP-1 also suffered testicular atrophy.
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