Journal
FEBS LETTERS
Volume 590, Issue 1, Pages 13-21Publisher
ELSEVIER SCIENCE BV
DOI: 10.1002/1873-3468.12030
Keywords
AKT; apoptosis; Bcl-2 family; mitochondria; yeast model
Funding
- Agence Nationale pour la Recherche (ANR project Phosbax) [ANR-12-ISV8-0002]
- Centre National de la Recherche Scientifique (CNRS)
- Fundacao para a Ciencia e a Tecnologia [FCT-ANR/BEX-BCM/0175/2012]
- FCT I.P. [UID/BIA/04050/2013]
- Fundação para a Ciência e a Tecnologia [FCT-ANR/BEX-BCM/0175/2012] Funding Source: FCT
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Bax-dependent mitochondrial permeabilization during apoptosis is controlled by multiple factors, including the phosphorylation by the protein kinase AKT. We used the heterologous co-expression of human Bax and AKT1 in yeast to investigate how the kinase modulates the different steps underlying Bax activation. We found that AKT activated Bax and increased its cellular content. Both effects were dependent on Ser184, but a phosphorylation of this residue did not fully explain the effects of AKT. Additional experiments with mutants substituted on Ser184 suggested that the regulation of Bax dynamic equilibrium between the cytosol and mitochondria might be more tightly regulated by Bcl-xL when Bax is phosphorylated.
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