PMID- 10075695
OWN - NLM
STAT- MEDLINE
DCOM- 19990415
LR  - 20190508
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 12
DP  - 1999 Mar 19
TI  - The cell death-promoting gene DP5, which interacts with the BCL2 family, is
      induced during neuronal apoptosis following exposure to amyloid beta protein.
PG  - 7975-81
AB  - 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-beta protein (A beta). DP5 mRNA was induced 6 h after treatment with A
      beta 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 beta. Moreover, DP5
      specifically interacts with Bcl-xl during neuronal apoptosis following exposure
      to A beta, 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
      beta.
FAU - Imaizumi, K
AU  - Imaizumi K
AD  - Department of Anatomy and Neuroscience, Osaka University Medical School, 2-2
      Yamadaoka, Suita, Osaka 565-0871, Japan. imaizumi@anat2.med.osaka-u.ac.jp
FAU - Morihara, T
AU  - Morihara T
FAU - Mori, Y
AU  - Mori Y
FAU - Katayama, T
AU  - Katayama T
FAU - Tsuda, M
AU  - Tsuda M
FAU - Furuyama, T
AU  - Furuyama T
FAU - Wanaka, A
AU  - Wanaka A
FAU - Takeda, M
AU  - Takeda M
FAU - Tohyama, M
AU  - Tohyama M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Hrk protein, rat)
RN  - 0 (Neuropeptides)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Alzheimer Disease/physiopathology
MH  - Amino Acid Sequence
MH  - Amyloid beta-Peptides/*pharmacology
MH  - Animals
MH  - *Apoptosis/genetics
MH  - Apoptosis Regulatory Proteins
MH  - Cells, Cultured
MH  - *Gene Expression Regulation
MH  - Molecular Sequence Data
MH  - Neurons/*physiology
MH  - Neuropeptides/*biosynthesis/*genetics
MH  - Protein Binding
MH  - Proto-Oncogene Proteins c-bcl-2/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
EDAT- 1999/03/13 00:00
MHDA- 1999/03/13 00:01
CRDT- 1999/03/13 00:00
PHST- 1999/03/13 00:00 [pubmed]
PHST- 1999/03/13 00:01 [medline]
PHST- 1999/03/13 00:00 [entrez]
AID - 10.1074/jbc.274.12.7975 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Mar 19;274(12):7975-81. doi: 10.1074/jbc.274.12.7975.