Requirement of the familial Alzheimer's disease gene PS2 for apoptosis. Opposing effect of ALG-3

Pasquale Vito, Benjamin Wolozin, J. Kelly Ganjei, Katsunori Iwasaki, Emanuela Lacaná, Luciano D'Adamio

Research output: Contribution to journalArticle

122 Scopus citations

Abstract

ALG-3, a truncated mouse homologue of the chromosome 1 familial Alzheimer's disease gene PS2, rescues T hybridoma 3DO cells from T-cell receptor-induced apoptosis by inhibiting Fas ligand induction and Fas signaling. Here we show that ALG-3 transfected 3DO cells express a COOH- terminal PS2 polypeptide. Overexpression of PS2 in ALG-3 transfected 3DO cells reconstitutes sensitivity to receptor-induced cell death, suggesting that the artificial PS2 polypeptide functions as a dominant negative mutant of PS2. ALG-3 and antisense PS2 protect PC12 cells from glutamate-induced apoptosis but not from death induced by hydrogen peroxide or the free radical MPP+. Thus, the PS2 gene is required for some forms of cell death in diverse cell types, and its function is opposed by ALG-3.

Original languageEnglish (US)
Pages (from-to)31025-31028
Number of pages4
JournalJournal of Biological Chemistry
Volume271
Issue number49
DOIs
StatePublished - Dec 17 1996

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Vito, P., Wolozin, B., Kelly Ganjei, J., Iwasaki, K., Lacaná, E., & D'Adamio, L. (1996). Requirement of the familial Alzheimer's disease gene PS2 for apoptosis. Opposing effect of ALG-3. Journal of Biological Chemistry, 271(49), 31025-31028. https://doi.org/10.1074/jbc.271.49.31025