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Disruption of the <i>ARF</i> transcriptional activator <i>DMP1</i> facilitates cell immortalization, Ras transformation, and tumorigenesis

Disruption of the ARF transcriptional activator DMP1 facilitates cell... Downloaded from genesdev.cshlp.org on July 31, 2022 - Published by Cold Spring Harbor Laboratory Press Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis 1 2 3 1,5 2 Kazushi Inoue, Renren Wen, Jerold E. Rehg, Masashi Adachi, John L. Cleveland, 1 1,4,6 Martine F. Roussel, and Charles J. Sherr 1 2 3 4 Departments of Tumor Cell Biology, Biochemistry, Pathology, and Howard Hughes Medical Institute, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105 USA The DMP1 transcription factor induces the ARF tumor suppressor gene in mouse fibroblasts, leading to cell cycle arrest in a p53-dependent manner. We disrupted sequences encoding the DNA-binding domain of DMP1 in mouse embryonic stem cells and derived animals lacking the functional protein. DMP1-null animals are small at birth, and males develop more slowly than their wild-type littermates. Some adult animals exhibit seizures and/or obstuctive uropathy, each of unknown cause. The growth of explanted DMP1-null mouse embryo fibroblasts (MEFs) is progressively retarded as cells are passaged in culture on defined transfer ARF protocols; but, unlike the behavior of normal cells, p19 , Mdm2, and p53 levels remain relatively low and DMP1-null MEFs do not senesce. Whereas the establishment of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

Disruption of the <i>ARF</i> transcriptional activator <i>DMP1</i> facilitates cell immortalization, Ras transformation, and tumorigenesis

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Unpaywall
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0890-9369
DOI
10.1101/gad.14.14.1797
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Abstract

Downloaded from genesdev.cshlp.org on July 31, 2022 - Published by Cold Spring Harbor Laboratory Press Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis 1 2 3 1,5 2 Kazushi Inoue, Renren Wen, Jerold E. Rehg, Masashi Adachi, John L. Cleveland, 1 1,4,6 Martine F. Roussel, and Charles J. Sherr 1 2 3 4 Departments of Tumor Cell Biology, Biochemistry, Pathology, and Howard Hughes Medical Institute, St. Jude Children’s Research Hospital, Memphis, Tennessee 38105 USA The DMP1 transcription factor induces the ARF tumor suppressor gene in mouse fibroblasts, leading to cell cycle arrest in a p53-dependent manner. We disrupted sequences encoding the DNA-binding domain of DMP1 in mouse embryonic stem cells and derived animals lacking the functional protein. DMP1-null animals are small at birth, and males develop more slowly than their wild-type littermates. Some adult animals exhibit seizures and/or obstuctive uropathy, each of unknown cause. The growth of explanted DMP1-null mouse embryo fibroblasts (MEFs) is progressively retarded as cells are passaged in culture on defined transfer ARF protocols; but, unlike the behavior of normal cells, p19 , Mdm2, and p53 levels remain relatively low and DMP1-null MEFs do not senesce. Whereas the establishment of

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Genes & Development – Unpaywall

Published: Jul 15, 2000

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