Please use this identifier to cite or link to this item: http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3467
Full metadata record
DC FieldValueLanguage
dc.creatorCerezo, Ana-
dc.creatorMartínez-Alonso, Carlos-
dc.creatorLanzarot, Diego-
dc.creatorFischer, Siegmund-
dc.creatorFranke, Thomas F.-
dc.creatorRebollo, Angelita-
dc.date2008-04-08T09:50:19Z-
dc.date2008-04-08T09:50:19Z-
dc.date1998-11-
dc.date.accessioned2017-01-31T01:01:37Z-
dc.date.available2017-01-31T01:01:37Z-
dc.identifierMolecular Biology of the Cell, Vol. 8, pp. 3107–3118, November 1998-
dc.identifier1059-1524-
dc.identifierhttp://hdl.handle.net/10261/3467-
dc.identifier.urihttp://dspace.mediu.edu.my:8181/xmlui/handle/10261/3467-
dc.descriptionEl copyright pertenece a The American Society for Cell Biology. The final versión of the paper is available at http://www.pubmedcentral.nih.gov-
dc.descriptionWe 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.descriptionPeer reviewed-
dc.format360048 bytes-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherAmerican Society for Cell Biology-
dc.rightsopenAccess-
dc.titleRole of Akt and c-Jun N-terminal Kinase 2 in Apoptosis Induced by Interleukin-4 Deprivation-
dc.typeArtículo-
Appears in Collections:Digital Csic

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.