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Titolo:
Status epilepticus induces p53 sequence-specific DNA binding in mature ratbrain
Autore:
Liu, W; Rong, YQ; Baudry, M; Schreiber, SS;
Indirizzi:
Univ So Calif, Sch Med, Dept Cell & Neurobiol, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 urobiol, Los Angeles, CA 90033 USA Univ So Calif, Program Neurobiol, Los Angeles, CA 90089 USA Univ So CalifLos Angeles CA USA 90089 urobiol, Los Angeles, CA 90089 USA
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 2, volume: 63, anno: 1999,
pagine: 248 - 253
SICI:
0169-328X(19990108)63:2<248:SEIPSD>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-DEATH; APOPTOSIS; PROTEIN; GENE; EXPRESSION; INDUCTION; ANTIGEN; NEURONS; ARREST; GADD45;
Keywords:
kainic acid; seizure; p53; DNA-binding; neuronal apoptosis; cycloheximide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Schreiber, SS Univ So Calif, Sch Med, Dept Neurol, 1333 San Pablo St,MCH142, Los Angeles, Univ So Calif 1333 San Pablo St,MCH142 Los Angeles CA USA 90033
Citazione:
W. Liu et al., "Status epilepticus induces p53 sequence-specific DNA binding in mature ratbrain", MOL BRAIN R, 63(2), 1999, pp. 248-253

Abstract

Previous studies have implicated the tumor suppressor gene, p53, in neuronal apoptosis due to excitotoxin treatment. To test whether p53 protein functions as a transcription factor during excitotoxic cell death, we used electrophoretic mobility shift assays to measure p53 sequence-specific DNA-binding activity following kainic acid (KA)-induced seizures. A rapid and significant increase in p53 DNA-binding activity was observed in extracts from kainate-vulnerable brain regions at 2.5 h after seizure onset, an effect which lasted up to 16 h after seizure-onset. DNA binding activity returned to normal by 30 h after KA injection. Pre-treatment with the protein synthesisinhibitor cycloheximide, as well as pre-incubation with PAb421, a p53 monoclonal antibody, significantly attenuated p53 DNA-binding activity induced by KA treatment. These results indicate that p53 protein may function as a transcription factor, following KA treatment, to regulate the expression ofp53-responsive genes involved in neuronal apoptosis. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 11:40:44