(Q28138711)

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The cell death-promoting gene DP5, which interacts with the BCL2 family, is induced during neuronal apoptosis following exposure to amyloid beta protein

scientific article (publication date: 19 March 1999)

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The cell death-promoting gene DP5, which interacts with the BCL2 family, is induced during neuronal apoptosis following exposure to amyloid beta protein (English)

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apoptotic process

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A Wanaka

7

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author name string

K Imaizumi

1

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T Morihara

2

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Y Mori

3

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T Katayama

4

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M Tsuda

5

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T Furuyama

6

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M Takeda

8

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M Tohyama

9

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publication date

19 March 1999

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Journal of Biological Chemistry

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274

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12

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7975-81

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Molecular cloning of a novel polypeptide, DP5, induced during programmed neuronal death

1 reference

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Expression pattern of a novel death-promoting gene, DP5, in the developing murine nervous system

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harakiri, a novel regulator of cell death, encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)

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Induction of apoptosis by human Nbk/Bik, a BH3-containing protein that interacts with E1B 19K

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BID: a novel BH3 domain-only death agonist

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Hydrogen peroxide mediates amyloid beta protein toxicity

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β-Amyloid polypeptide increases calcium-uptake in PC12 cells: a possible mechanism for its cellular toxicity in Alzheimer's disease

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Secreted forms of beta-amyloid precursor protein protect hippocampal neurons against amyloid beta-peptide-induced oxidative injury

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Apoptosis is induced by beta-amyloid in cultured central nervous system neurons

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Apoptosis in the pathogenesis and treatment of disease

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Role of Ca2+ channels in the ability of membrane depolarization to prevent neuronal death induced by trophic-factor deprivation: evidence that levels of internal Ca2+ determine nerve growth factor dependence of sympathetic ganglion cells

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Evidence that nerve growth factor dependence of sympathetic neurons for survival in vitro may be determined by levels of cytoplasmic free Ca2+.

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Multiple calcium channels and neuronal function

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Increased intracellular Ca2+: a critical link in the pathophysiology of sepsis?

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Ecdysone-inducible gene expression in mammalian cells and transgenic mice.

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Altered gene expression in neurons during programmed cell death: identification of c-jun as necessary for neuronal apoptosis

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Calcium-destabilizing and neurodegenerative effects of aggregated beta-amyloid peptide are attenuated by basic FGF.

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bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death

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Evidence that BCL-2 represses apoptosis by regulating endoplasmic reticulum-associated Ca2+ fluxes

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Maintenance of calcium homeostasis in the endoplasmic reticulum by Bcl-2

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Inhibition of Bax channel-forming activity by Bcl-2

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Apoptosis mediated neurotoxicity induced by chronic application of beta amyloid fragment 25-35.

1 reference

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Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene

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Linker histones, DNA's protein custodians, gain new respect

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21 January 2018

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10.1074/JBC.274.12.7975

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