Abstract:
:We have shown previously that interleukin-4 (IL-4) protects TS1alphabeta cells from apoptosis, but very little is known about the mechanism by which IL-4 exerts this effect. We found that Akt activity, which is dependent on phosphatidylinositol 3 kinase, is reduced in IL-4-deprived TS1alphabeta cells. Overexpression of wild-type Akt or a constitutively active Akt mutant protects cells from IL-4 deprivation-induced apoptosis. Readdition of IL-4 before the commitment point is able to restore Akt activity. We also show expression and c-Jun N-terminal kinase 2 activation after IL-4 deprivation. Overexpression of the constitutively activated Akt mutant in IL-4-deprived cells correlates with inhibition of c-Jun N-terminal kinase 2 activity. Finally, TS1alphabeta survival is independent of Bcl-2, Bcl-x, or Bax.
journal_name
Mol Biol Celljournal_title
Molecular biology of the cellauthors
Cerezo A,Martínez-A C,Lanzarot D,Fischer S,Franke TF,Rebollo Adoi
10.1091/mbc.9.11.3107subject
Has Abstractpub_date
1998-11-01 00:00:00pages
3107-18issue
11eissn
1059-1524issn
1939-4586journal_volume
9pub_type
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