Inhibition of fas death signals by FLIPs.

Détails

ID Serval
serval:BIB_E59DFB495E51
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Inhibition of fas death signals by FLIPs.
Périodique
Current Opinion in Immunology
Auteur⸱e⸱s
Tschopp J., Irmler M., Thome M.
ISSN
0952-7915 (Print)
ISSN-L
0952-7915
Statut éditorial
Publié
Date de publication
1998
Volume
10
Numéro
5
Pages
552-558
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Résumé
The death receptor Fas is a member of the tumor necrosis factor receptor family; upon interaction with its ligand it efficiently activates caspases and induces apoptosis. Despite abundant Fas surface expression, however, Fas death-signals are frequently interrupted. Many viruses express antiapoptotic proteins, including caspase inhibitors, Bcl-2 homologues and death-effector-domain-containing proteins that are termed FLIPs (FLICE [Fas-associated death-domain-like IL-1beta-converting enzyme]-inhibitory proteins). Cellular homologues of these inhibitors have been identified. Cellular FLIPs structurally resemble caspase-8 except that they lack proteolytic activity. FLIPs are highly expressed in tumor cells, T lymphocytes and healthy, but not injured, myocytes; this suggests a critical role of FLIPs as endogenous modulators of apoptosis.
Mots-clé
Animals, Antigens, CD95/physiology, Apoptosis, CASP8 and FADD-Like Apoptosis Regulating Protein, Carrier Proteins/physiology, Caspase Inhibitors, Caspases/physiology, Fas Ligand Protein, Humans, Intracellular Signaling Peptides and Proteins, Membrane Glycoproteins/physiology, Proto-Oncogene Proteins c-bcl-2/physiology
Pubmed
Web of science
Création de la notice
24/01/2008 15:18
Dernière modification de la notice
20/08/2019 16:09
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