ERK and cell death: Mechanisms of ERK-induced cell death - apoptosis, autophagy and senescence

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,...

Full description

Saved in:
Bibliographic Details
Published in:The FEBS journal 2010-01, Vol.277 (1), p.2-21
Main Authors: Cagnol, Sebastien, Chambard, Jean-Claude
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - physiology
autophagy
Autophagy - physiology
Biochemistry
Caspase 8 - physiology
Cell Death - physiology
Cellular biology
Cellular Senescence - physiology
Cytochromes c - physiology
DUSP
ERK
Extracellular Signal-Regulated MAP Kinases - physiology
Humans
Kinases
Lysosomes - physiology
MAP Kinase Signaling System
Models, Biological
Proto-Oncogene Proteins c-bcl-2 - physiology
raf Kinases - physiology
ras Proteins - physiology
Reactive Oxygen Species - metabolism
ROS
senescence
Signal transduction
Tumor Suppressor Protein p53 - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1742-464X
1742-4658
DOI:10.1111/j.1742-4658.2009.07366.x