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Reversible abrogation of IL-3 dependence by an inducible H-ras oncogene.

1989; Springer Nature; Volume: 8; Issue: 9 Linguagem: Inglês

10.1002/j.1460-2075.1989.tb08396.x

1460-2075

E. Andrejauskas, Christoph Moroni,

Virus-based gene therapy research

Research Article1 September 1989free access Reversible abrogation of IL-3 dependence by an inducible H-ras oncogene. E. Andrejauskas E. Andrejauskas Institute for Medical Microbiology, University of Basel, Switzerland. Search for more papers by this author C. Moroni C. Moroni Institute for Medical Microbiology, University of Basel, Switzerland. Search for more papers by this author E. Andrejauskas E. Andrejauskas Institute for Medical Microbiology, University of Basel, Switzerland. Search for more papers by this author C. Moroni C. Moroni Institute for Medical Microbiology, University of Basel, Switzerland. Search for more papers by this author Author Information E. Andrejauskas1 and C. Moroni1 1Institute for Medical Microbiology, University of Basel, Switzerland. The EMBO Journal (1989)8:2575-2581https://doi.org/10.1002/j.1460-2075.1989.tb08396.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Immortalized, interleukin-3 (IL-3)-dependent mouse mast cells (PB-3c) were transfected with a human activated c-H-ras gene under the transcriptional control of the mouse mammary tumor virus long terminal repeat. Addition of increasing amounts of dexamethasone resulted in a concentration-dependent increase in expression of the H-ras oncogene. The elevation of p21 ras protein concentrations was paralleled by progressive growth of the transfectants in the absence of exogenous IL-3, leading to complete abrogation of growth-factor requirement at high p21ras levels. The maintenance of the IL-3-independent state required the continuous expression of the H-ras oncogene, since dexamethasone removal was followed by rapid cell death. Expression of the H-ras oncogene induced PB-3c cells to produce IL-3 and granulocyte-macrophage colony-stimulating factor, suggesting that their IL-3-independent proliferation may be due to an autocrine mechanism. Previous ArticleNext Article Volume 8Issue 91 September 1989In this issue RelatedDetailsLoading ...