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• W284493936 abstract "Research Article1 September 1995free access Activating point mutations in the common beta subunit of the human GM-CSF, IL-3 and IL-5 receptors suggest the involvement of beta subunit dimerization and cell type-specific molecules in signalling. B. J. Jenkins B. J. Jenkins Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author R. D'Andrea R. D'Andrea Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author T. J. Gonda T. J. Gonda Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author B. J. Jenkins B. J. Jenkins Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author R. D'Andrea R. D'Andrea Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author T. J. Gonda T. J. Gonda Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. Search for more papers by this author Author Information B. J. Jenkins1, R. D'Andrea1 and T. J. Gonda1 1Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Frome Road, Adelaide, SA, Australia. The EMBO Journal (1995)14:4276-4287https://doi.org/10.1002/j.1460-2075.1995.tb00102.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info We have combined retroviral expression cloning with random mutagenesis to identify two activating point mutations in the common signal-transducing subunit (h beta c) of the receptors for human granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-3 and IL-5 by virtue of their ability to confer factor independence on the haemopoietic cell line, FDC-P1. One mutation (V449E) is located within the transmembrane domain and, by analogy with a similar mutation in the neu oncogene, may act by inducing dimerization of h beta c. The other mutation (I374N) lies in the extracellular, membrane-proximal portion of h beta c. Neither of these mutants, nor a previously described mutant of h beta c (FI delta, which has a small duplication in the extracellular region), was capable of inducing factor independence in CTLL-2 cells, while only V449E could induce factor independence in BAF-B03 cells. These results imply that the extracellular and transmembrane mutations act by different mechanisms. Furthermore, they imply that the mutants, and hence also wild-type h beta c, interact with cell type-specific signalling molecules. Models are presented which illustrate how these mutations may act and predict some of the characteristics of the putative receptor-associated signalling molecules. Previous ArticleNext Article Volume 14Issue 171 September 1995In this issue RelatedDetailsLoading ..." @default.
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• W284493936 date "1995-09-01" @default.
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• W284493936 title "Activating point mutations in the common beta subunit of the human GM-CSF, IL-3 and IL-5 receptors suggest the involvement of beta subunit dimerization and cell type-specific molecules in signalling." @default.
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• W284493936 doi "https://doi.org/10.1002/j.1460-2075.1995.tb00102.x" @default.
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