Nerve growth factor attenuates endoplasmic reticulum stress-mediated apoptosis via suppression of caspase-12 activity.
J Biochem
; 135(3): 439-46, 2004 Mar.
Article
em En
| MEDLINE
| ID: mdl-15113843
ABSTRACT
Following endoplasmic reticulum (ER) stress, which occurs via inhibition of the glycosylation of newly synthesized proteins, caspase family proteins are activated to promote ER stress-mediated apoptosis. Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Detailed analysis of the mechanism underlying the NGF-mediated cell survival revealed that the activities of all seriate caspases were reduced through the phosphatidylinositol 3-kinase (PI3-K) signaling pathway induced by NGF. Moreover, we found that the activity of c-Jun N-terminal kinase (JNK) was not essential for the tunicamycin-induced apoptosis of PC12 cells. These results demonstrate that the inactivation of caspase-12 via the NGF-mediated PI3-K signaling pathway leads to inactivation of the caspase cascade including caspase-3 and -9.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Apoptose
/
Fator de Crescimento Neural
/
Retículo Endoplasmático
/
Inibidores de Caspase
Limite:
Animals
Idioma:
En
Revista:
J Biochem
Ano de publicação:
2004
Tipo de documento:
Article