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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Role of Akt and c-Jun N-terminal kinase 2 in apoptosis induced by interleukin-4 deprivation.

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.[1]

References

  1. Role of Akt and c-Jun N-terminal kinase 2 in apoptosis induced by interleukin-4 deprivation. Cerezo, A., Martínez-A, C., Lanzarot, D., Fischer, S., Franke, T.F., Rebollo, A. Mol. Biol. Cell (1998) [Pubmed]
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