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Titolo:
Pro-apoptotic effects of tau mutations in chromosome 17 frontotemporal dementia and parkinsonism
Autore:
Furukawa, K; DSouza, I; Crudder, CH; Onodera, H; Itoyama, Y; Poorkaj, P; Bird, TD; Schellenberg, GD;
Indirizzi:
Vet Affairs Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle Div, Seattle, WA 98108 USA Vet Affairs Puget Sound Hlth Care Syst Seattle WA USA 98108 WA 98108 USA Univ Washington, Dept Neurol & Pharmacol, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 l & Pharmacol, Seattle, WA 98195 USA Univ Washington, Div Gerontol & Geriatr Med, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 & Geriatr Med, Seattle, WA 98195 USA Tohoku Univ, Sch Med, Dept Neurol, Aoba Ku, Sendai, Miyagi 9808574, Japan Tohoku Univ Sendai Miyagi Japan 9808574 Ku, Sendai, Miyagi 9808574, Japan
Titolo Testata:
NEUROREPORT
fascicolo: 1, volume: 11, anno: 2000,
pagine: 57 - 60
SICI:
0959-4965(20000117)11:1<57:PEOTMI>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTECTS HIPPOCAMPAL-NEURONS; EXCITOTOXICITY; FTDP-17; GENE;
Keywords:
apoptosis; calcium; frontotemporal dementia and parkinsonism; mutation; tau;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
8
Recensione:
Indirizzi per estratti:
Indirizzo: Furukawa, K Vet Affairs Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ &Clin, Seattle Div, Seattle, WA 98108 USA Vet Affairs Puget Sound Hlth CareSyst Seattle WA USA 98108 A
Citazione:
K. Furukawa et al., "Pro-apoptotic effects of tau mutations in chromosome 17 frontotemporal dementia and parkinsonism", NEUROREPORT, 11(1), 2000, pp. 57-60

Abstract

It was recently discovered that mutations of tau cause hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Here werepels that cultured SH-SY5Y human neuroblastoma cells transfected with mutated tau genes are more vulnerable to apoptotic stimulus. Two kinds of mutations of tau causing FTDP-17 were examined in the present study: one was in exon 10 (N279K) and the other was in exon 12 (V337M). SH-SY5Y cells transfected with either mutated tau were more vulnerable to serum withdrawal, whereas cells transfected with the wild-type tau or vector alone showed no significant change in apoptotic vulnerability. The increase in the intracellular calcium concentration by the serum withdrawal was significantly greaterin the SH-SY5Y cells transfected with mutated tau genes than in cells transfected with the wild-type tau or vector alone. These results suggest that mutations of tau might cause FTDP-17 by these proapoptotic functions by disrupting the intracellular calcium homeostasis. NeuroReport 11:57-60 (C) 2000 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/21 alle ore 04:11:50