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Publication : Induction of ARF tumor suppressor gene expression and cell cycle arrest by transcription factor DMP1.

First Author  Inoue K Year  1999
Journal  Proc Natl Acad Sci U S A Volume  96
Issue  7 Pages  3993-8
PubMed ID  10097151 Mgi Jnum  J:54019
Mgi Id  MGI:1334012 Doi  10.1073/pnas.96.7.3993
Citation  Inoue K, et al. (1999) Induction of ARF tumor suppressor gene expression and cell cycle arrest by transcription factor DMP1. Proc Natl Acad Sci U S A 96(7):3993-8
abstractText  Expression of the DMP1 transcription factor, a cyclin D-binding Myb-like protein, induces growth arrest in mouse embryo fibroblast strains but is devoid of antiproliferative activity in primary diploid fibroblasts that lack the ARF tumor suppressor gene. DMP1 binds to a single canonical recognition site in the ARF promoter to activate gene expression, and in turn, p19(ARF) synthesis causes p53-dependent cell cycle arrest. Unlike genes such as Myc, adenovirus E1A, and E2F-1, which, when overexpressed, activate the ARF-p53 pathway and trigger apoptosis, DMP1, like ARF itself, does not induce programmed cell death. Therefore, apart from its recently recognized role in protecting cells from potentially oncogenic signals, ARF can be induced in response to antiproliferative stimuli that do not obligatorily lead to apoptosis.
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