In:
Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 63, No. 2 ( 1998-02-01), p. 253-263
Abstract:
We demonstrate a rapid and transient activation of phosphoinositide-3-kinase (PI-3-K) by Fas receptor triggering or cellular treatment with synthetic C6-ceramide. The stimulation of PI-3-K is critical for Fas or C6-ceramide-induced programmed cell death because transfection with a transdominant inhibitory PI-3-K construct or pretreatment with the PI-3-K inhibitor wortmannin almost completely prevented Fas or C6-ceramide-mediated apoptosis. Treatment with the caspase inhibitor Ac-YVAD-cmk or cellular transfection with transdominant inhibitory N17Ras prevented PI-3-K stimulation by Fas, suggesting that Fas activates PI-3-K via caspases and Ras. N17Ras expression also prevented C6-ceramide-initiated PI-3-K stimulation. The notion of a PI-3-K regulation by Ras upon Fas receptor ligation or ceramide treatment is supported by co-immunoprecipitation experiments revealing an activation-dependent association of PI-3-K and Ras.
Type of Medium:
Online Resource
ISSN:
0741-5400
,
1938-3673
DOI:
10.1002/jlb.63.2.253
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
1998
detail.hit.zdb_id:
2026833-6
SSG:
12
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