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Control of cell cycle progression by c-Jun is p53 dependent

Control of cell cycle progression by c-Jun is p53 dependent Downloaded from genesdev.cshlp.org on September 18, 2021 - Published by Cold Spring Harbor Laboratory Press Control of cell cycle progression by c-Jun is p53 dependent 1,4 2 3,5 2 1 Martin Schreiber, Andrea Kolbus, Fabrice Piu, Axel Szabowski, Uta Mo ¨ hle-Steinlein, 3 3 2 1,6 Jianmin Tian, Michael Karin, Peter Angel, and Erwin F. Wagner 1 2 Research Institute of Molecular Pathology (IMP), A-1030 Vienna, Austria; Deutsches Krebsforschungszentrum (DKFZ), Division of Signal Transduction and Growth Control, D-69120 Heidelberg, Germany; Department of Pharmacology, University of California at San Diego, La Jolla, California 92093-0636 USA The c-jun proto-oncogene encodes a component of the mitogen-inducible immediate–early transcription factor AP-1 and has been implicated as a positive regulator of cell proliferation and G -to-S-phase progression. Here −/− we report that fibroblasts derived from c-jun mouse fetuses exhibit a severe proliferation defect and undergo a prolonged crisis before spontaneous immortalization. The cyclin D1- and cyclin E-dependent kinases (CDKs) and transcription factor E2F are poorly activated, resulting in inefficient G -to-S-phase progression. Furthermore, the absence of c-Jun results in elevated expression of the tumor suppressor gene p53 and its target gene, the CDK inhibitor p21, whereas overexpression of c-Jun represses p53 and p21 expression http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

Control of cell cycle progression by c-Jun is p53 dependent

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Unpaywall
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0890-9369
DOI
10.1101/gad.13.5.607
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Abstract

Downloaded from genesdev.cshlp.org on September 18, 2021 - Published by Cold Spring Harbor Laboratory Press Control of cell cycle progression by c-Jun is p53 dependent 1,4 2 3,5 2 1 Martin Schreiber, Andrea Kolbus, Fabrice Piu, Axel Szabowski, Uta Mo ¨ hle-Steinlein, 3 3 2 1,6 Jianmin Tian, Michael Karin, Peter Angel, and Erwin F. Wagner 1 2 Research Institute of Molecular Pathology (IMP), A-1030 Vienna, Austria; Deutsches Krebsforschungszentrum (DKFZ), Division of Signal Transduction and Growth Control, D-69120 Heidelberg, Germany; Department of Pharmacology, University of California at San Diego, La Jolla, California 92093-0636 USA The c-jun proto-oncogene encodes a component of the mitogen-inducible immediate–early transcription factor AP-1 and has been implicated as a positive regulator of cell proliferation and G -to-S-phase progression. Here −/− we report that fibroblasts derived from c-jun mouse fetuses exhibit a severe proliferation defect and undergo a prolonged crisis before spontaneous immortalization. The cyclin D1- and cyclin E-dependent kinases (CDKs) and transcription factor E2F are poorly activated, resulting in inefficient G -to-S-phase progression. Furthermore, the absence of c-Jun results in elevated expression of the tumor suppressor gene p53 and its target gene, the CDK inhibitor p21, whereas overexpression of c-Jun represses p53 and p21 expression

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Genes & Development – Unpaywall

Published: Mar 1, 1999

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