| Literature DB >> 16337592 |
Barbara Nicke1, Julie Bastien, Sophia J Khanna, Patricia H Warne, Victoria Cowling, Simon J Cook, Gordon Peters, Oona Delpuech, Almut Schulze, Katrien Berns, Jasper Mullenders, Roderick L Beijersbergen, René Bernards, Trivadi S Ganesan, Julian Downward, David C Hancock.
Abstract
The ability of activated Ras to induce growth arrest of human ovarian surface epithelial (HOSE) cells via induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) has been used to screen for Ras pathway signaling components using a library of RNA interference (RNAi) vectors targeting the kinome. Two known Ras-regulated kinases were identified, phosphoinositide 3-kinase p110alpha and ribosomal protein S6 kinase p70(S6K1), plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras signaling. MINK is activated after Ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 MAPK downstream of the Raf/ERK pathway. p38 MAPK activation is essential for Ras-induced p21(WAF1/CIP1) upregulation and cell cycle arrest. MINK is thus a distal target of Ras signaling in the induction of a growth-arrested, senescent-like phenotype that may act to oppose oncogenic transformation in HOSE cells.Entities:
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Year: 2005 PMID: 16337592 DOI: 10.1016/j.molcel.2005.10.038
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970