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Role of Akt and c-Jun N-terminal Kinase 2 in Apoptosis Induced by Interleukin-4 Deprivation

AuthorsCerezo, Ana; Martínez-Alonso, Carlos; Lanzarot, Diego; Fischer, Siegmund; Franke, Thomas F.; Rebollo, Angelita
Issue DateNov-1998
PublisherAmerican Society for Cell Biology
CitationMolecular Biology of the Cell, Vol. 8, pp. 3107–3118, November 1998
AbstractWe have shown previously that interleukin-4 (IL-4) protects TS1ab 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 TS1ab 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, TS1ab survival is independent of Bcl-2, Bcl-x, or Bax.
DescriptionEl copyright pertenece a The American Society for Cell Biology. The final versión of the paper is available at
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