Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Chronic ethanol exposure enhances activating protein-1 transcriptional activity in human neuroblastoma cells
Autore:
Fried, U; Kotarsky, K; Alling, C;
Indirizzi:
Lund Univ, Inst Lab Med, Dept Med Neurochem, S-22185 Lund, Sweden Lund Univ Lund Sweden S-22185 , Dept Med Neurochem, S-22185 Lund, Sweden Lund Univ, Dept Physiol Sci, Div Mol Neurobiol, S-22362 Lund, Sweden Lund Univ Lund Sweden S-22362 i, Div Mol Neurobiol, S-22362 Lund, Sweden
Titolo Testata:
ALCOHOL
fascicolo: 3, volume: 24, anno: 2001,
pagine: 189 - 195
SICI:
0741-8329(200107)24:3<189:CEEEAP>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBELLAR GRANULE CELLS; RAT-BRAIN; C-FOS; KINASE-C; GENE-EXPRESSION; NERVOUS-SYSTEM; JUN; WITHDRAWAL; AP-1; IMMUNOREACTIVITY;
Keywords:
ethanol; activating protein-1; protein kinase C; mitogen-activated protein kinases; reporter gene; SH-SY5Y;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Fried, U Lund Univ, Inst Lab Med, Dept Med Neurochem, S-22185 Lund, SwedenLund Univ Lund Sweden S-22185 d Neurochem, S-22185 Lund, Sweden
Citazione:
U. Fried et al., "Chronic ethanol exposure enhances activating protein-1 transcriptional activity in human neuroblastoma cells", ALCOHOL, 24(3), 2001, pp. 189-195

Abstract

This study demonstrates a method for studying the effects of ethanol on transcription mediated by activating protein-1 (AP-1). The effects of ethanolon AP-1 activity and on the signaling cascades in this process were investigated by using a reporter gene technique with secreted alkaline phosphatase as the reporter gene coupled to nine DNA AP-1-binding elements. Long-termethanol exposure (48-72 h) dose dependently enhanced AP-1 transcriptional activity in SH-SY5Y cells. Shorter exposure periods with ethanol did not influence AP-1 transcriptional activity compared with findings for control cells. Inhibition of protein kinase C (PKC) dramatically decreased AP-1 activity in both control and ethanol-exposed cells and abolished the ethanol enhancement. This finding suggests a pivotal role for PKC-coupled signaling inAP-1 transcriptional activity. Phorbol ester stimulation of AP-1 transcriptional activity was not influenced by long-term ethanol exposure. This finding indicates that signaling events upstream of PKC are the targets for ethanol. Mitogen-activated protein kinases ERK and p38 may play a role in ethanol-enhanced AP-I activity because inhibitors of both enzymes partly reduced the enhancement. The inhibitors also partly blocked phorbol ester-inducedAP-1 activation, which demonstrates a function of these mitogen-activated protein kinases downstream of PKC. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 00:10:26