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Titolo:
Brain-derived neurotrophic factor stimulates beta-amyloid gene promoter activity by a Ras-dependent/AP-1-independent mechanism in SH-SY5Y neuroblastoma cells
Autore:
Ruiz-Leon, Y; Pascual, A;
Indirizzi:
CSIC, Inst Invest Biomed, E-28029 Madrid, Spain CSIC Madrid Spain E-28029 SIC, Inst Invest Biomed, E-28029 Madrid, Spain
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 2, volume: 79, anno: 2001,
pagine: 278 - 285
SICI:
0022-3042(200110)79:2<278:BNFSBG>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; PRECURSOR PROTEIN GENE; INDUCED NEURONAL DIFFERENTIATION; CEREBELLAR GRANULE NEURONS; ALZHEIMERS-DISEASE; TRANSCRIPTIONAL ACTIVITY; MESSENGER-RNA; RESPONSIVE ELEMENT; SIGNALING PATHWAYS; BINDING DOMAIN;
Keywords:
beta-amyloid precursor protein (APP); brain-derived neurotrophic factor; neuroblastoma cells; promoter; protein kinase C; Ras;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Pascual, A CSIC, Inst Invest Biomed, Arturo Duperier 4, E-28029 Madrid, Spain CSIC Arturo Duperier 4 Madrid Spain E-28029 8029 Madrid, Spain
Citazione:
Y. Ruiz-Leon e A. Pascual, "Brain-derived neurotrophic factor stimulates beta-amyloid gene promoter activity by a Ras-dependent/AP-1-independent mechanism in SH-SY5Y neuroblastoma cells", J NEUROCHEM, 79(2), 2001, pp. 278-285

Abstract

The beta -amyloid peptide, the major component of Alzheimer-associated plaques, derives from a larger p-amyloid precursor protein (APP), that is expressed in both neural and non-neural cells. Overexpression of APP actively contributes to the development of senile plaques and is considered a risk factor for the disease. APP expression is regulated by a variety of cellular mediators, among them ligands of tyrosine kinase receptors. In this study, we present evidence that brain-derived neurotrophic factor (BDNF) modulates, in a dose- and time-dependent fashion, APP promoter activity in SH-SY5Y neuroblastoma. cells transiently expressing the receptor TrkB. The APP promoter contains two potential AP-1 sites, and we examined whether or not protein kinase C (PKC) and the AP-1 sites of the promoter mediate the BDNF-induced stimulation of APP. Stimulation of APP promoter activity by BDNF was notaffected by the PKC inhibitor bisindolylmaleimide, or by dominant negativemutants of the AP-1 components Fos and Jun, which, however, blocked the response to phorbol esters. These results suggest that activation of the APP promoter by BDNF is largely independent of PKC and AP-1. In contrast, activated Ras increased APP promoter activity in SH-SY5Y cells, and a dominant negative mutant of Ras abolished BDNF-mediated promoter stimulation. Taken together, our results suggest a mechanism that involves activation of the Ras/MAP kinase signaling pathway, and phosphorylation of as yet unidentified effectors which in turn can activate response elements within the APP promoter.

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Documento generato il 01/04/20 alle ore 23:16:34