Advances in Research on Neurodegeneration: Volume 7 by C. L. Wellington, B. R. Leavitt (auth.), Prof. Y. Mizuno,

By C. L. Wellington, B. R. Leavitt (auth.), Prof. Y. Mizuno, Prof. D. B. Calne, Dr. R. Horowski, Prof. W. Poewe, Prof. P. Riederer, Prof. M. B. H. Youdim (eds.)

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Sch. Med, B. Elibol at the Dept. Neurol. Faculty Med. Hacettepe Univ, AJ. Brookes at the Dept. Med. , Biomed. Center. This work was supported in part by the grants from the Ministry of Education, Science, Sports and Culture, Japan Society of Promotion of Science , and the National Parkinson Foundation. PARKIN as a pathogenic gene for autosomal recessive juvenile parkinsonism 29 References Asakawa S, Abe I, Kudoh Y, Kishi N, Wang Y, Kubota R, Kudoh J, Kawasaki K, Minoshima S, Shimizu N (1997) Human BAC library: construction and screening.

Faculty Med. Hacettepe Univ, AJ. Brookes at the Dept. Med. , Biomed. Center. This work was supported in part by the grants from the Ministry of Education, Science, Sports and Culture, Japan Society of Promotion of Science , and the National Parkinson Foundation. PARKIN as a pathogenic gene for autosomal recessive juvenile parkinsonism 29 References Asakawa S, Abe I, Kudoh Y, Kishi N, Wang Y, Kubota R, Kudoh J, Kawasaki K, Minoshima S, Shimizu N (1997) Human BAC library: construction and screening.

1997). Thus, one of the major function of Bel-2 in the established neurons in adults might be to protect these cells from accidental or chronic insults. , 1996). Function of BcI-2 family proteins in regulating apoptosis A variety of apoptotic stimuli commonly activate caspases that eleave critical cellular proteins, leading to apoptosis. Bel-2 prevents cell death by blocking a step leading to the activation of caspases (Green and Reed, 1998). Concerning how Bel-2 prevents the activation of caspases, basically two independent mechanisms have been considered, which are schematically summarized in Fig.

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