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A short cytoplasmic domain of the amyloid precursor protein induces apoptosis in vitro and in vivo.

Bertrand, Eric, Brouillet, Emmanuel, Caillé, Isabelle, Bouillot, Colette, Cole, Greg M., Prochiantz, Alain, Allinquant, Bernadette·2001·Molecular and Cellular Neuroscience
DOI 10.1006/mcne.2001.1030
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Abstract

The amyloid precursor protein presents several cleavage sites leading to the release of its entire C-terminal domain into the cytoplasm. During apoptosis, this C-terminal domain can be cleaved at amino acid 664 by caspases 3, 6, and 8 and can thus generate two peptides N- and C-terminal to amino acid 664 (C31). Recently, it was shown that the C31 induces apoptosis after transfection into N2A and 293 T cell lines. We have analyzed here, by internalization into neurons, the physiological consequences of the entire C-terminal domain (APP-Cter) and of its membrane proximal sequence corresponding to the N-terminal peptide unmasked after caspase cleavage. We find that whereas micromolar concentrations of APP-Cter are harmless, the peptide extending from the membrane (amino acid 649) to the caspase cleavage site (amino acid 664) in the same range of concentrations induces DNA fragmentation, cleavage of actin at a caspase-sensitive site, and activates caspase 3. A mutated version of this sequence (tyrosine 653 replaced by an aspartate) abolishes the effect in vitro and in vivo. Taken together, this report suggests the existence of a new mechanism contributing to Alzheimer's Disease-associated cell death.

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  • When γ-secretase processes C99 into Aβ, the remaining AICD is further cleaved by caspase to generate C31 and JCasp fragments, both of which promote neuronal apoptosis.

    “When γ-secretase processes C99 into Aβ, the remaining AICD is further cleaved by caspase to generate C31 and JCasp fragments, both of which promote neuronal apoptosis (Bertrand et al., 2001; Madeira et al., 2005).”

    From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Bertrand et al., 2001

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Metadata

Authors
Bertrand, E., Brouillet, E., Caillé, I., Bouillot, C., Cole, G. M., Prochiantz, A., & Allinquant, B.
Venue
Molecular and Cellular Neuroscience
Publisher
Elsevier BV
Published
2001-11
Volume
18
Issue
5
Pages
503-511
ISSN
1044-7431
DOI
10.1006/mcne.2001.1030
Cited by
69
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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