The Roles of SEK1 in Nitric Oxide (NO) Induced Apoptsis of RAW264.7 cells / 대한면역학회지
Korean Journal of Immunology
;
: 55-61, 1999.
Artículo
en Coreano
| WPRIM
| ID: wpr-181226
ABSTRACT
Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To elucidate the roles of SEK1/MKK4, a upstream kinase for both c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 kinase, on NO-induced apoptosis, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-Kl) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-Kl) with sodium nitroprusside (SNP), a NO generating agent, significantly decreased the cell viability up to 20% of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. For a while, caspase-3 like activity in NO treated RAW/SEK1-Kl cells was significantly increased with parallell to apoptotic death rate. However, caspase1 like activity was not affected by NO in any transfectants. The NO induced apoptosis in RAW/SEK1-Kl cells was significantly prevented by the addition of caspase-3 like inhibitor (N-Ac- DEVD-CHO). In addition, the phosphotransferase activity of JNK1 in NO-treated RAW/SEK1-WT is significantly increased, but not in RAW/SEK1-Kl cells. These results suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fosfotransferasas
/
Proteínas Quinasas
/
Nitroprusiato
/
Supervivencia Celular
/
Mortalidad
/
Muerte Celular
/
Células Clonales
/
Apoptosis
/
Caspasa 3
/
Macrófagos
Tipo de estudio:
Estudio pronóstico
Idioma:
Coreano
Revista:
Korean Journal of Immunology
Año:
1999
Tipo del documento:
Artículo
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