Possible involvement of both mitochondria- and endoplasmic reticulum-dependent caspase pathways in rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells
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Acknowledgements
We thank Mr D. Tsuchiya and Ms K. Nakamura for their technical assistance. The present study was supported in part by the Frontier Research Program (T.T.); Grants-in-Aid (Y.K., T.T., Y.N., S.S.) from the Ministry of Education, Science, Sports and Culture of Japan; and a Grant-in-Aid for the promotion of the advancement of education and research in graduate schools (Special Research) from the Promotion and Mutual Aid Corporation for Private Schools of Japan (T.T.).
References (19)
- et al.
Glycoxidation and oxidative stress in Parkinson disease and diffuse Lewy body disease
Brain Res.
(1996) - et al.
Parkin suppresses unfolded protein stress-induced cell death through its E3 ubiquitin-protein ligase activity
J. Biol. Chem.
(2000) - et al.
An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of Parkin
Cell
(2001) - et al.
Nitric oxide donor-induced p53-sensitive cell death is enhanced by Bcl-2 reduction in human neuroblastoma cells
Neurochem. Int.
(1998) - et al.
Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
Cell
(1997) - et al.
Coupling endoplasmic reticulum stress to the cell death program: mechanism of caspase activation
J. Biol. Chem.
(2001) - et al.
Coupling endoplasmic reticulum stress to the cell death program: an Apaf-1-independent intrinsic pathway
J. Biol. Chem.
(2002) - et al.
Mitochondrial complex I deficiency in Parkinson's disease
Lancet
(1989) - et al.
Apaf-1, a human protein homologous to C, elegans CED-4, participates in cytochrome c-dependent activation of caspase-3
Cell
(1997)
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