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Titolo:
E2F1 mediates death of B-amyloid-treated cortical neurons in a manner independent of p53 and dependent on Bax and caspase 3
Autore:
Giovanni, A; Keramaris, E; Morris, EJ; Hou, ST; OHare, M; Dyson, N; Robertson, GS; Slack, RS; Park, DS;
Indirizzi:
Univ Ottawa, Neurosci Res Inst, Ottawa, ON K1H 8M5, Canada Univ Ottawa Ottawa ON Canada K1H 8M5 Res Inst, Ottawa, ON K1H 8M5, Canada Hoechst Marion Roussel, Neurosci, Bridgewater, NJ 08807 USA Hoechst MarionRoussel Bridgewater NJ USA 08807 Bridgewater, NJ 08807 USA Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA Massachusetts Gen Hosp Charlestown MA USA 02129 Charlestown, MA 02129 USA Natl Res Council Canada, Inst Biol Sci, Ottawa, ON K1A 0R6, Canada Natl Res Council Canada Ottawa ON Canada K1A 0R6 tawa, ON K1A 0R6, Canada Merck Frosst, Pointe Claire, PQ H9R 4P8, Canada Merck Frosst Pointe Claire PQ Canada H9R 4P8 e Claire, PQ H9R 4P8, Canada
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 16, volume: 275, anno: 2000,
pagine: 11553 - 11560
SICI:
0021-9258(20000421)275:16<11553:EMDOBC>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALZHEIMERS-DISEASE BRAIN; ABL TYROSINE KINASE; CELL-CYCLE; RETINOBLASTOMA PROTEIN; BETA-PEPTIDE; TRANSCRIPTION FACTOR; INDUCED APOPTOSIS; TRANSGENIC MICE; NERVOUS-SYSTEM; RB;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Park, DS Univ Ottawa, Neurosci Res Inst, Ottawa, ON K1H 8M5, Canada Univ Ottawa Ottawa ON Canada K1H 8M5 Ottawa, ON K1H 8M5, Canada
Citazione:
A. Giovanni et al., "E2F1 mediates death of B-amyloid-treated cortical neurons in a manner independent of p53 and dependent on Bax and caspase 3", J BIOL CHEM, 275(16), 2000, pp. 11553-11560

Abstract

Although B-amyloid (AB) is suggested to play an important role in Alzheimer's disease, the mechanisms that control AB-evoked toxicity are unclear. Wedemonstrated previously that the cell cycle-related cyclin-dependent kinase 4/6/retinoblastoma protein pathway is required for AB-mediated death. However, the downstream target(s) of this pathway are unknown. We show here that neurons lacking E2F1, a transcription factor regulated by the retinoblastoma protein, are significantly protected from death evoked by AB, Moreover, p53 deficiency does not protect neurons from death, indicating that E2F1-mediated death occurs independently of p53. Neurons protected by E2F1 deficiency have reduced Bax-dependent caspase 3-like activity. However, protection afforded by E2F1, Bax, or caspase 3 deficiency is transient. In the caseof E2F1, but not with Bax or caspase 3 deficiency, delayed death is accompanied by DEVD-AFC cleavage activity. Taken together, these results demonstrate the required role of E2F1, Bax, and caspase 3 in AB evoked death, but also suggest the participation of elements independent of these apoptosis regulators.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 20:50:52