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ERK and cell death: Mechanisms of ERK‐induced cell death – apoptosis, autophagy and senescence
Author(s) -
Cagnol Sebastien,
Chambard JeanClaude
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2009.07366.x
Subject(s) - mapk/erk pathway , microbiology and biotechnology , autophagy , programmed cell death , apoptosis , senescence , biology , kinase , mitochondrion , signal transduction , intracellular , chemistry , biochemistry
The Ras/Raf/extracellular signal‐regulated kinase (ERK) signaling pathway plays a crucial role in almost all cell functions and therefore requires exquisite control of its spatiotemporal activity. Depending on the cell type and stimulus, ERK activity will mediate different antiproliferative events, such as apoptosis, autophagy and senescence in vitro and in vivo . ERK activity can promote either intrinsic or extrinsic apoptotic pathways by induction of mitochondrial cytochrome c release or caspase‐8 activation, permanent cell cycle arrest or autophagic vacuolization. These unusual effects require sustained ERK activity in specific subcellular compartments and could depend on the presence of reactive oxygen species. We will summarize the mechanisms involved in Ras/Raf/ERK antiproliferative functions.