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

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Vol. 9, Issue 11, 3107-3118, November 1998

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

Ana Cerezo,^* Carlos Martínez-A,^* Diego Lanzarot,^* Siegmund Fischer, Thomas F. Franke, and Angelita Rebollo^*^§

^*Department of Immunology and Oncology, Centro Nacional de Biotecnología, Universidad Autónoma, Campus de Cantoblanco, E-28049 Madrid, Spain; Laboratoire d'Oncologie Cellulaire et Moleculaire, Institut National de la Santé et de la Recherche Médicale-363, Hôpital Cochin, F-75014 Paris, France; and Department of Pharmacology, Columbia University, New York, New York 10032

We have shown previously that interleukin-4 (IL-4) protects TS1 $alpha$ $beta$ cells from apoptosis, but very little is known about themechanism by which IL-4 exerts this effect. We found that Aktactivity, which is dependent on phosphatidylinositol 3 kinase,is reduced in IL-4-deprived TS1 $alpha$ $beta$ cells. Overexpression of wild-typeAkt or a constitutively active Akt mutant protects cells fromIL-4 deprivation-induced apoptosis. Readdition of IL-4 beforethe commitment point is able to restore Akt activity. We alsoshow expression and c-Jun N-terminal kinase 2 activation afterIL-4 deprivation. Overexpression of the constitutively activatedAkt mutant in IL-4-deprived cells correlates with inhibition ofc-Jun N-terminal kinase 2 activity. Finally, TS1 $alpha$ $beta$ survival isindependent of Bcl-2, Bcl-x, orBax.

^§ Corresponding author. E-mail address: arebollo{at}cnb.uam.es.

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