期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 100, 期 26, 页码 15930-15935出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2536808100
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资金
- NCI NIH HHS [P30 CA021765, R01 CA076379, CA21765, CA71907, CA76379, T32 CA070089, P01 CA071907, T32-CA70089] Funding Source: Medline
- NIDDK NIH HHS [DK44158, F32-DK10154, F32 DK010154, R01 DK044158] Funding Source: Medline
induction of the Arf tumor suppressor gene by elevated thresholds of mitogenic signals activates a p53-dependent transcriptional response that triggers either growth arrest or apoptosis, thereby countering abnormal cell proliferation. Conversely, Arf inactivation is associated with tumor development. Expression of Arf in tissues of adult mice is difficult to detect, possibly because its induction leads to the arrest or elimination of incipient tumor cells. We replaced coding sequences of exon 1beta of the mouse cellular Arf gene with a cDNA encoding GFP, thereby producing Arf-null animals in which GFP expression is driven by the intact Arf promoter. The Arf promoter was induced in several biologic settings previously shown to elicit mouse p19(Arf) expression. Inactivation of Arf in this manner led to the outgrowth of tumor cells expressing GFP, thereby providing direct evidence that the Arf promoter monitors latent oncogenic signals in vivo.
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