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Titolo:
Insulin-like growth factor I (IGF-I) protects cells from apoptosis by Alzheimer's V642I mutant amyloid precursor protein through IGF-I receptor in anIGF-binding protein-sensitive manner
Autore:
Niikura, T; Hashimoto, Y; Okamoto, T; Abe, Y; Yasukawa, T; Kawasumi, M; Hiraki, T; Kita, Y; Terashita, K; Kouyama, K; Nishimoto, I;
Indirizzi:
Keio Univ, Sch Med, Dept Pharmacol & Neurosci, Shinjuku Ku, Tokyo 1608582,Japan Keio Univ Tokyo Japan 1608582 Neurosci, Shinjuku Ku, Tokyo 1608582,Japan RIKEN, Brain Sci Inst, Wako, Saitama 3510198, Japan RIKEN Wako Saitama Japan 3510198 n Sci Inst, Wako, Saitama 3510198, Japan
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 6, volume: 21, anno: 2001,
pagine: 1902 - 1910
SICI:
0270-6474(20010315)21:6<1902:IGFI(P>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROTROPHIC FACTOR ADNF; SOMATOMEDIN-C LEVELS; PC12 CELLS; HIPPOCAMPAL-NEURONS; FACTOR DEPRIVATION; OXIDATIVE STRESS; BETA-PROTEIN; PHOSPHATIDYLINOSITOL 3-KINASE; SYMPATHETIC NEURONS; KINASE-ACTIVITY;
Keywords:
IGF-I; IGFBP; des(1-3)IGF-I; amyloid precursor protein; Alzheimer's disease; neuroprotection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Nishimoto, I Keio Univ, Sch Med, Dept Pharmacol & Neurosci, Shinjuku Ku, Tokyo 1608582,Japan Keio Univ Tokyo Japan 1608582 njuku Ku, Tokyo 1608582,Japan
Citazione:
T. Niikura et al., "Insulin-like growth factor I (IGF-I) protects cells from apoptosis by Alzheimer's V642I mutant amyloid precursor protein through IGF-I receptor in anIGF-binding protein-sensitive manner", J NEUROSC, 21(6), 2001, pp. 1902-1910

Abstract

It has been found that insulin-like growth factor I (IGF-I) exerts cytoprotection against A beta amyloid-induced neuronal cell death. Deposits of A beta amyloid are one of the pathological hallmarks of Alzheimer's disease (AD). Here, we examined whether IGF-I exerts protective activity against celldeath induced by a familial AD (FAD)-linked mutant of amyloid precursor protein (APP), and we found that IGF-I protected cells from toxicity of FAD-associated V642I mutant of APP in multiple cell systems. IGFBP-3 blocked this action of IGF-I, but not of des( 1-3) IGF-I, which was as active as IGF-Iin the presence of IGFBP-3. The data also demonstrated that the IGF-I receptor (IGF-IR) mediates the protective activity of IGF-I. The antagonizing function of the IGF-I/IGF-IR system against V642I-APP, which is further antagonized by IGFBP-3, provides a molecular clue to the understanding of AD pathophysiology and to the establishment of potential therapy for AD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 02:31:36