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J Biol Chem, Vol. 274, Issue 12, 7975-7981, March 19, 1999
Protein
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From the Departments of DP5, which contains a BH3 domain, was cloned as a
neuronal apoptosis-inducing gene. To confirm that DP5 interacts with
members of the Bcl-2 family, 293T cells were transiently co-transfected with DP5 and Bcl-xl cDNA constructs, and immunoprecipitation was carried out. The 30-kDa Bcl-xl was co-immunoprecipitated with Myc-tagged DP5, suggesting that DP5 physically interacts with Bcl-xl in
mammalian cells. Previously, we reported that DP5 is induced during
neuronal apoptosis in cultured sympathetic neurons. Here, we analyzed
DP5 gene expression and the specific interaction of DP5 with Bcl-xl
during neuronal death induced by amyloid- Anatomy and Neuroscience and
** Neuropsychiatry, Osaka University Medical School, 2-2 Yamadaoka,
Suita, Osaka 565-0871, Japan, § Tanabe Seiyaku Co. Ltd.,
3-16-89 Kashima, Yodogawaku, Osaka 532-0031, Japan, the
Institute of Biomedical Sciences, Fukushima
Medical College, Fukushima 960-1247, Japan, and ¶ Core Research
for Evolutional Science and Technology (CREST),
Kawaguchi 332-0012, Japan
protein (A ). DP5
mRNA was induced 6 h after treatment with A in cultured
rat cortical neurons. The protein encoded by DP5 mRNA showed a
specific interaction with Bcl-xl. Induction of DP5 gene expression was
blocked by nifedipine, an inhibitor of L-type voltage-dependent calcium channels, and dantrolene, an
inhibitor of calcium release from the endoplasmic reticulum. These
results suggested that the induction of DP5 mRNA occurs downstream
of the increase in cytosolic calcium concentration caused by A . Moreover, DP5 specifically interacts with Bcl-xl during neuronal apoptosis following exposure to A , and its binding could impair the
survival-promoting activities of Bcl-xl. Thus, the induction of DP5
mRNA and the interaction of DP5 and Bcl-xl could play significant roles in neuronal degeneration following exposure to A .
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