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

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...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, No. 7 (1999), p. 3993-8
Main Author: Inoue, K
Other Involved Persons: Roussel, M F ; Sherr, C J
Format: Article
Language:English
ISSN:1091-6490
Item Description:Date Completed 12.05.1999
Date Revised 01.05.2019
published: Print
Citation Status MEDLINE
Copyright: From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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  • 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