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The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

SET protein (TAF1β, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain

Madeira, Alexandra, Pommet, Jean‐Michel, Prochiantz, Alain, Allinquant, Bernadette·2005·The FASEB Journal
DOI 10.1096/fj.05-3839fje
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Abstract

When overexpressed, a short cytoplasmic domain of the amyloid precursor protein (APP), normally unmasked in the brain of Alzheimer's disease patients, activates caspase‐3 and induces neuronal death. Death induction by this “Jcasp” domain is lost when tyrosine 653 is changed into an aspartate, suggesting specific interactions with unknown partners. To identify these putative partners and start to elucidate the mechanisms involved in Jcasp‐induced cell death, we internalized a biotinylated version of the peptide into primary neurons and analyzed intracellular interacting proteins by pull‐down and mass spectrometry. We find that SET protein, also called template‐activating factor (TAF1β) or phosphatase 2A inhibitor 2 (I 2 PP2A ), specifically binds Jcasp early after internalization and that SET and Jcasp interact directly in vitro. Down‐regulation of SET reduces Jcasp‐induced cell death, confirming a role of this protein in Jcasp‐induced apoptosis. Conversely, SET gain of function increases cell death, which suggests that SET level is crucial for neuronal survival/death. Taken together, these results suggest that SET is part of a neuronal apoptotic pathway related to Alzheimer's disease and provides a new entry in the analysis of this pathology.

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Crossref · 10.1096/fj.05-3839fje

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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 Madeira et al., 2005

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Research works printed but not linked: 48

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Metadata

Authors
Madeira, A., Pommet, J., Prochiantz, A., & Allinquant, B.
Affiliations
  • INSERM U 573 Centre Paul Broca 2 ter rue d'Alésia 75014 Paris France
  • CNRS UMR 8542 ENS 46 rue d'Ulm 75005 Paris France
Venue
The FASEB Journal
Publisher
Wiley
Published
2005-09-14
Volume
19
Issue
13
Pages
1905-1907
ISSN
  • 0892-6638
  • 1530-6860
DOI
10.1096/fj.05-3839fje
Cited by
102
References
3
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
  • College of Natural Resources and Sciences, Humboldt State University
  • Institut National de la Santé et de la Recherche Médicale
  • Fondation pour la Recherche Médicale
  • Association France Alzheimer

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