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Titolo:
Increased expression of Fas (CD95/APO-I) in adult rat brain after kainate-induced seizures
Autore:
Tan, ZQ; Levid, J; Schreiber, SS;
Indirizzi:
Univ So Calif, Keck Sch Med, Dept Neurol, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 Neurol, Los Angeles, CA 90033 USA Univ So Calif, Keck Sch Med, Dept Cell & Neurobiol, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 urobiol, Los Angeles, CA 90033 USA
Titolo Testata:
NEUROREPORT
fascicolo: 9, volume: 12, anno: 2001,
pagine: 1979 - 1982
SICI:
0959-4965(20010703)12:9<1979:IEOF(I>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-DEATH; APOPTOSIS; ANTIGEN; LIGAND; ACCUMULATION; HIPPOCAMPUS; INDUCTION; NECROSIS; ISCHEMIA; BINDING;
Keywords:
apoptosis; excitotoxicity; Fas; kainic acid; neurodegeneration; seizures;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Schreiber, SS Univ So Calif, Keck Sch Med, Dept Neurol, 1333 San Pablo St MCH 142, Los Angeles, CA 90033 USA Univ So Calif 1333 San Pablo St MCH 142 Los Angeles CA USA 90033
Citazione:
Z.Q. Tan et al., "Increased expression of Fas (CD95/APO-I) in adult rat brain after kainate-induced seizures", NEUROREPORT, 12(9), 2001, pp. 1979-1982

Abstract

Fas (CD95/APO-1), a transmembrane glycoprotein and receptor for the Fas ligand, plays an important role in apoptosis. The present study examined whether excitotoxic cell death induces Fas expression in the adult rat brain. Although relatively light immunostaining was observed in control brain sections, significantly increased Fas immunoreactivity was seen from 4 h to 5 days after the onset of kainic acid-induced seizures. Increased expression ofboth Fas mRNA and protein were also evident by reverse transcription polymerase chain reaction and Western blotting, respectively. Fas induction was correlated with neuronal apoptosis as demonstrated by colocalization of Fasand terminal dT-mediated dUTP nick end-labeling (TUNEL). Cells with increased Fas-expression were also immunoreactive for tumor suppressor p53 and neuronal specific nuclear protein (NeuN). These results suggest chat Fas receptor may contribute to excitotoxic neuronal death in cooperation with p53, and further implicates the Fas pathway in the pathophysiology of neurodegenerative diseases. NeuroReport 12:1979-1982 (C) 2001 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 11:52:34