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Titolo:
Zinc enhances synthesis of presenilin 1 in mouse primary cortical culture
Autore:
Park, IH; Jung, MW; Mori, H; Mook-Jung, I;
Indirizzi:
Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 442721, South Korea Ajou Univ Suwon South Korea 442721 is Res Ctr, Suwon 442721, South Korea Ajou Univ, Sch Med, Inst Med Sci, Suwon 442721, South Korea Ajou Univ Suwon South Korea 442721 st Med Sci, Suwon 442721, South Korea Osaka City Univ, Sch Med, Dept Neurosci, Osaka 5458585, Japan Osaka City Univ Osaka Japan 5458585 Dept Neurosci, Osaka 5458585, Japan
Titolo Testata:
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
fascicolo: 3, volume: 285, anno: 2001,
pagine: 680 - 688
SICI:
0006-291X(20010720)285:3<680:ZESOP1>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID PRECURSOR PROTEIN; GAMMA-SECRETASE ACTIVITY; HISTOCHEMICALLY-REACTIVE ZINC; ALZHEIMER A-BETA; TRANSGENIC MICE; DISEASE; NEURONS; BRAIN; ENDOPROTEOLYSIS; APOPTOSIS;
Keywords:
Alzheimer's disease; presenilin 1; zinc; beta amyloid; cell death; TPEN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Mook-Jung, I Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 442721, South Korea Ajou Univ Suwon South Korea 442721 uwon 442721, South Korea
Citazione:
I.H. Park et al., "Zinc enhances synthesis of presenilin 1 in mouse primary cortical culture", BIOC BIOP R, 285(3), 2001, pp. 680-688

Abstract

Whether zinc interacts with presenilin 1 (PS1), one of the causative genesof familial Alzheimer's disease (AD), is not known. Here we report that zinc modulates the synthesis of PSI. Exogenous zinc enhanced the amount of C-terminal fragments of PS1 (PS1-CTF) in neonatal mouse cortical cultures in a dose-dependent manner. Zinc also induced cell death in a dose-dependent manner. These effects of zinc were not mimicked by calcium, copper, or iron,and were blocked by a zinc-specific chelator, TPEN. Experiments using metabolic labeling and cycloheximide treatment revealed that zinc increased PS1-CTF by elevating the de novo synthesis of PS1. Time course experiments revealed that cell death commenced sooner (0.5-1 h) than enhancement of PS1-CTF (1-2 h) following zinc treatment. However, the amount of PS1-CTF remainedunchanged during etoposide- or H2O2-induced cell death, suggesting that enhancement of PSI synthesis is specifically correlated with zinc-induced cell death. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 00:47:07