PI3K/Akt promotes GRP78 accumulation and inhibits endoplasmic reticulum stress-induced apoptosis in HEK293 cells.
Folia Biol (Praha)
; 56(2): 37-46, 2010.
Article
em En
| MEDLINE
| ID: mdl-20492754
ABSTRACT
The potential pro-survival role of phosphatidylinositol 3-kinase (PI3K)/Akt during endoplasmic reticulum stress has been well-characterized. However, the detailed mechanisms remain largely unknown. Here, we showed that PI3K/Akt inhibition promoted endoplasmic reticulum stress-induced apoptosis in a glucose-regulated protein 78 (GRP78)-dependent manner. During endoplasmic reticulum stress, high levels of Akt phosphorylation were sustained for at least 18 h in HEK293 cells. Importantly, PI3K/Akt enhanced GRP78 accumulation through increasing its stability following endoplasmic reticulum stress. Furthermore, Akt1, but not Akt2 or Akt3, was involved in GRP78 stability regulation. These results suggest that PI3K/Akt inhibits endoplasmic reticulum stress-induced apoptosis in HEK293 cells, at least in part, by promoting GRP78 protein stability.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estresse Fisiológico
/
Apoptose
/
Fosfatidilinositol 3-Quinases
/
Retículo Endoplasmático
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Proteínas Proto-Oncogênicas c-akt
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Proteínas de Choque Térmico
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Folia Biol (Praha)
Ano de publicação:
2010
Tipo de documento:
Article