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Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK... Downloaded from genesdev.cshlp.org on November 24, 2021 - Published by Cold Spring Harbor Laboratory Press Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling 1 2 3 1 2 Athena W. Lin, Marta Barradas, James C. Stone, Linda van Aelst, Manuel Serrano, 1,4 and Scott W. Lowe 1 2 Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 USA; Department of Immunology and Oncology, Centro Nacional de Biotecnologa ´ , Cantoblanco, Madrid E-28049, Spain; Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2H7, Canada Oncogenic Ras transforms immortal rodent cells to a tumorigenic state, in part, by constitutively transmitting mitogenic signals through the mitogen-activated protein kinase (MAPK) cascade. In primary cells, Ras is INK4a initially mitogenic but eventually induces premature senescence involving the p53 and p16 tumor suppressors. Constitutive activation of MEK (a component of the MAPK cascade) induces both p53 and p16, and is required for Ras-induced senescence of normal human fibroblasts. Furthermore, activated MEK permanently arrests primary murine fibroblasts but forces uncontrolled mitogenesis and transformation in cells lacking either p53 or INK4a. The precisely opposite response of normal and immortalized cells to constitutive activation of the MAPK cascade implies http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

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Unpaywall
ISSN
0890-9369
DOI
10.1101/gad.12.19.3008
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Abstract

Downloaded from genesdev.cshlp.org on November 24, 2021 - Published by Cold Spring Harbor Laboratory Press Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling 1 2 3 1 2 Athena W. Lin, Marta Barradas, James C. Stone, Linda van Aelst, Manuel Serrano, 1,4 and Scott W. Lowe 1 2 Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724 USA; Department of Immunology and Oncology, Centro Nacional de Biotecnologa ´ , Cantoblanco, Madrid E-28049, Spain; Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2H7, Canada Oncogenic Ras transforms immortal rodent cells to a tumorigenic state, in part, by constitutively transmitting mitogenic signals through the mitogen-activated protein kinase (MAPK) cascade. In primary cells, Ras is INK4a initially mitogenic but eventually induces premature senescence involving the p53 and p16 tumor suppressors. Constitutive activation of MEK (a component of the MAPK cascade) induces both p53 and p16, and is required for Ras-induced senescence of normal human fibroblasts. Furthermore, activated MEK permanently arrests primary murine fibroblasts but forces uncontrolled mitogenesis and transformation in cells lacking either p53 or INK4a. The precisely opposite response of normal and immortalized cells to constitutive activation of the MAPK cascade implies

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Genes & Development – Unpaywall

Published: Oct 1, 1998

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