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Titolo:
ICE-PROTEASE INHIBITORS BLOCK MURINE LIVER-INJURY AND APOPTOSIS CAUSED BY CD95 OR BY TNF-ALPHA
Autore:
KUNSTLE G; LEIST M; UHLIG S; REVESZ L; FEIFEL R; MACKENZIE A; WENDEL A;
Indirizzi:
UNIV KONSTANZ,FAC BIOL,DEPT BIOCHEM PHARMACOL,POB 5560 M667 D-78434 CONSTANCE GERMANY UNIV KONSTANZ,FAC BIOL,DEPT BIOCHEM PHARMACOL D-78434 CONSTANCE GERMANY UNIV KONSTANZ,FAC BIOL,DEPT MOL TOXICOL D-78434 CONSTANCE GERMANY SANDOZ PHARMA LTD,PRECLIN RES CH-4002 BASEL SWITZERLAND
Titolo Testata:
Immunology letters
fascicolo: 1, volume: 55, anno: 1997,
pagine: 5 - 10
SICI:
0165-2478(1997)55:1<5:IIBMLA>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; DEATH GENE CED-3; CELL-DEATH; INTERLEUKIN-1-BETA-CONVERTING ENZYME; IL-1-BETA-CONVERTING ENZYME; ICE/CED-3 PROTEASE; FAS ANTIGEN; HEPATITIS-C; RECEPTOR; ENCODES;
Keywords:
CPP32; INTERLEUKIN-1-BETA CONVERTING ENZYME; FAS/APO-1; TNF; ICE-LIKE PROTEASES; CASPASES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
28
Recensione:
Indirizzi per estratti:
Citazione:
G. Kunstle et al., "ICE-PROTEASE INHIBITORS BLOCK MURINE LIVER-INJURY AND APOPTOSIS CAUSED BY CD95 OR BY TNF-ALPHA", Immunology letters, 55(1), 1997, pp. 5-10

Abstract

The two apoptosis receptors of mammalian cells, i.e. the 55 kDa TNF receptor (TNF-R1) and CD95 (Fas/APO1) are activated independently of each other, however, their signaling involves a variety of ICE-related proteases [1]. We used a cell-permeable inhibitor of ICE-like protease activity to examine in vivo whether post-receptor signaling of TNF andCD95 are fully independent processes. Mice pretreated with the inhibitor, Z-VAD-fluoromethylketone (FMK) were dose-dependently protected from liver injury caused by CD95 activation as determined by plasma alanine aminotransferase and also from hepatocyte apoptosis assessed by DNA fragmentation (ID50 = 0.1 mg/kg). A dose of 10 mg/kg protected mice also from liver injury induced by TNF-alpha. Similar results were found when apoptosis was initiated via TNF-alpha or via CD95 in primary murine hepatocytes (IC50 = 1.5 nM) or in various human cell lines. In addition to prevention, an arrest of cell death by Z-VAD-FMK was demonstrated in vivo and in vitro after stimulation of apoptosis receptors. These findings show in vitro and in vivo in mammals that CD95 and the TNF-alpha receptor share a distal proteolytic apoptosis signal. (C) 1997 Elsevier Science B.V.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:03:36