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Article Dans Une Revue European Journal of Immunology Année : 2011

Actin-independent exclusion of CD95 by PI3K/AKT signalling: implications for apoptosis.

Résumé

The immune system eliminates infected or transformed cells through the activation of the death receptor CD95. CD95 engagement drives the recruitment of the adaptor protein Fas-associated death domain protein (FADD), which in turn aggregates and activates initiator caspases-8 and -10. The CD95-mediated apoptotic signal relies on the capacity to form the CD95/FADD/caspases complex termed the death-inducing signalling complex (DISC). Cells are classified according to the magnitude of DISC formation as either type I (efficient DISC formation) or type II (inefficient). CD95 localised to lipid rafts in type I cells, whereas the death receptor was excluded from these domains in type II cells. Here, we show that inhibition of both PI3K class IA and serine-threonine kinase Akt in type II cells promoted the redistribution of CD95 into lipid rafts, DISC formation and the initiation of the apoptotic signal. Strikingly, these molecular events took place independently of CD95L and the actin cytoskeleton. Overall, these findings highlight that the oncogenic PI3K/Akt signalling pathway participates in maintaining cells in a type II phenotype by excluding CD95 from lipid rafts.

Domaines

Immunologie
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Dates et versions

hal-00680900 , version 1 (20-03-2012)

Identifiants

Citer

Mathieu Pizon, Hariniaina Rampanarivo, Sébastien Tauzin, Benjamin Chaigne-Delalande, Sophie Daburon, et al.. Actin-independent exclusion of CD95 by PI3K/AKT signalling: implications for apoptosis.. European Journal of Immunology, 2011, 41 (8), pp.2368-78. ⟨10.1002/eji.201041078⟩. ⟨hal-00680900⟩
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