noc-18 and geranylgeranylacetone

noc-18 has been researched along with geranylgeranylacetone* in 1 studies

Other Studies

1 other study(ies) available for noc-18 and geranylgeranylacetone

Article	Year
Geranylgeranylacetone induces apoptosis in HL-60 cells. Cell structure and function, 1999, Volume: 24, Issue:3 Geranylgeranylacetone (GGA) induces apoptosis in human leukemia HL-60 cells in a dose- and time-dependent manner. This effect was completely prevented by the pan-caspase inhibitor z-Val-Ala-Asp(OMe) fluoromethylketone, thereby implicating the caspase cascade in the process. Prior to DNA fragmentation, GGA treatment markedly activated caspase-3(-like) proteases, which might be responsible for the observed apoptosis. In addition, GGA treatment interfered with the processing and membrane localization of Rap1 and Ras, and these changes may be a result of apoptosis. Moreover, nitric oxide donors significantly accentuated the GGA-induced apoptosis, suggesting that the apoptotic pathway induced by GGA might be regulated by a redox-sensitive mechanism. Taken together, these data suggest that the isoprenoid, GGA, is an effective inducer of apoptotic cell death in HL-60 cells. Topics: Amino Acid Chloromethyl Ketones; Apoptosis; bcl-2-Associated X Protein; Blotting, Western; Caspases; Diterpenes; DNA Fragmentation; DNA-Binding Proteins; Dose-Response Relationship, Drug; HL-60 Cells; Humans; Multigene Family; Nitroso Compounds; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; ras Proteins; Subcellular Fractions	1999

Article

Year

Geranylgeranylacetone induces apoptosis in HL-60 cells.

Cell structure and function, 1999, Volume: 24, Issue:3

Geranylgeranylacetone (GGA) induces apoptosis in human leukemia HL-60 cells in a dose- and time-dependent manner. This effect was completely prevented by the pan-caspase inhibitor z-Val-Ala-Asp(OMe) fluoromethylketone, thereby implicating the caspase cascade in the process. Prior to DNA fragmentation, GGA treatment markedly activated caspase-3(-like) proteases, which might be responsible for the observed apoptosis. In addition, GGA treatment interfered with the processing and membrane localization of Rap1 and Ras, and these changes may be a result of apoptosis. Moreover, nitric oxide donors significantly accentuated the GGA-induced apoptosis, suggesting that the apoptotic pathway induced by GGA might be regulated by a redox-sensitive mechanism. Taken together, these data suggest that the isoprenoid, GGA, is an effective inducer of apoptotic cell death in HL-60 cells.

Topics: Amino Acid Chloromethyl Ketones; Apoptosis; bcl-2-Associated X Protein; Blotting, Western; Caspases; Diterpenes; DNA Fragmentation; DNA-Binding Proteins; Dose-Response Relationship, Drug; HL-60 Cells; Humans; Multigene Family; Nitroso Compounds; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; ras Proteins; Subcellular Fractions

1999