作者: Ok-Jin Han , Keun Ho Joe , Seong Won Kim , Hee Sung Lee , Nyoun Soo Kwon
关键词: p38 mitogen-activated protein kinases 、 Protein kinase A 、 Cell culture 、 Kinase 、 ASK1 、 MAP kinase kinase kinase 、 Programmed cell death 、 Biology 、 Cell biology 、 Apoptosis
摘要: Although nitric oxide (NO) plays key signaling roles in the nervous systems, excess NO leads to cell death. In this study, involvement of p38 mitogen-activated protein kinase (p38 MAPK) and apoptosis signal-regulating kinase-1 (ASK1) NO-induced death was investigated PC12 cells. donor transiently activated MAPK wild type parental cells, whereas activation abolished NO-resistant cells (PC12-NO-R). inhibitors protected against death, were not significantly protective cytotoxicity reactive oxygen species. Stable transfection with dominant negative mutant reduced ASK1 attenuated NO-stimulated decreased These results suggest that its upstream regulator are involved