cFLIP regulation of lymphocyte activation and development

Détails

ID Serval
serval:BIB_C9272FC055BC
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
cFLIP regulation of lymphocyte activation and development
Périodique
Nature Reviews. Immunology
Auteur⸱e⸱s
Budd  R. C., Yeh  W. C., Tschopp  J.
ISSN
1474-1733 (Print)
Statut éditorial
Publié
Date de publication
03/2006
Volume
6
Numéro
3
Pages
196-204
Notes
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review --- Old month value: Mar
Résumé
Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling through competition with caspase-8 for recruitment to FAS-associated via death domain (FADD). More recently, it has been determined that both cFLIP and caspase-8 are required for the survival and proliferation of T cells following T-cell-receptor stimulation. This paradoxical finding launched new investigations of how these molecules might connect with signalling pathways that link to cell survival and growth following antigen-receptor activation. As discussed in this Review, insight gained from these studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell-receptor signalling to activation of nuclear factor-kappaB through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor-interacting protein 1 (RIP1).
Mots-clé
Animals Antigens, CD95/physiology Autoimmunity CASP8 and FADD-Like Apoptosis Regulating Protein Humans Intracellular Signaling Peptides and Proteins/chemistry/genetics/*physiology *Lymphocyte Activation Neoplasms/etiology T-Lymphocytes/immunology/*physiology
Pubmed
Web of science
Création de la notice
24/01/2008 15:19
Dernière modification de la notice
20/08/2019 15:44
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