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Research Database PMU-SQQUID

The actin cytoskeleton, RAS-cAMP signaling and mitochondrial ROS in yeast apoptosis.
Breitenbach, M; Laun, P; Gimona, M;
Trends Cell Biol. 2005; 15(12): 637-639.
Kurzberichte/Notes

PMU-Authors

Gimona Mario

Abstract

The release of reactive oxygen species (ROS) by mitochondria instigates the pathways of programmed cell death in eukaryotic cells. Gourlay and Ayscough present intriguing experimental evidence that mutations in the genes encoding the regulatory proteins End3p and Sla1p, which influence actin dynamics in budding yeast, lead to a loss of mitochondrial membrane potential, resulting in ROS production and apoptosis. This effect can be suppressed by down-regulation of the RAS-cAMP signaling pathway, thus establishing the existence of a new and complex regulatory network.


Useful keywords (using NLM MeSH Indexing)

Actins/analysis

Actins/physiology*

Apoptosis/physiology*

Carrier Proteins/genetics

Carrier Proteins/physiology

Cyclic AMP/physiology*

Cytoskeletal Proteins/genetics

Cytoskeletal Proteins/physiology

Cytoskeleton/chemistry

Cytoskeleton/physiology*

Gene Expression Regulation, Fungal

Genes, ras/genetics

Genes, ras/physiology

Membrane Potentials/physiology

Mitochondria/metabolism*

Mutation

Reactive Oxygen Species/metabolism*

Saccharomyces cerevisiae/cytology*

Saccharomyces cerevisiae/physiology

Saccharomyces cerevisiae Proteins/genetics

Saccharomyces cerevisiae Proteins/physiology

Signal Transduction/physiology*

ras Proteins/physiology*