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

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dc.creator Cerezo, Ana
dc.creator Martínez-Alonso, Carlos
dc.creator Lanzarot, Diego
dc.creator Fischer, Siegmund
dc.creator Franke, Thomas F.
dc.creator Rebollo, Angelita
dc.date 2008-04-08T09:50:19Z
dc.date 2008-04-08T09:50:19Z
dc.date 1998-11
dc.date.accessioned 2017-01-31T01:01:37Z
dc.date.available 2017-01-31T01:01:37Z
dc.identifier Molecular Biology of the Cell, Vol. 8, pp. 3107–3118, November 1998
dc.identifier 1059-1524
dc.identifier http://hdl.handle.net/10261/3467
dc.identifier.uri http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3467
dc.description El copyright pertenece a The American Society for Cell Biology. The final versión of the paper is available at http://www.pubmedcentral.nih.gov
dc.description We 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.
dc.description Peer reviewed
dc.format 360048 bytes
dc.format application/pdf
dc.language eng
dc.publisher American Society for Cell Biology
dc.rights openAccess
dc.title Role of Akt and c-Jun N-terminal Kinase 2 in Apoptosis Induced by Interleukin-4 Deprivation
dc.type Artículo


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