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https://hdl.handle.net/2440/8785
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dc.contributor.author | Jenkins, B. | - |
dc.contributor.author | D'Andrea, R. | - |
dc.contributor.author | Gonda, T. | - |
dc.date.issued | 1995 | - |
dc.identifier.citation | The EMBO Journal, 1995; 14(17):4276-4287 | - |
dc.identifier.issn | 0261-4189 | - |
dc.identifier.issn | 1460-2075 | - |
dc.identifier.uri | http://hdl.handle.net/2440/8785 | - |
dc.description.abstract | 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. | - |
dc.description.statementofresponsibility | Jenkins, B J ; D'andrea, R ; Gonda, T J | - |
dc.language.iso | en | - |
dc.publisher | IRL Press | - |
dc.source.uri | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC394511/ | - |
dc.subject | Hematopoietic Stem Cells | - |
dc.subject | Cell Line | - |
dc.subject | Animals | - |
dc.subject | Humans | - |
dc.subject | Mice | - |
dc.subject | Cell Transformation, Neoplastic | - |
dc.subject | Macromolecular Substances | - |
dc.subject | Receptors, Granulocyte-Macrophage Colony-Stimulating Factor | - |
dc.subject | Receptors, Interleukin-3 | - |
dc.subject | Receptors, Interleukin | - |
dc.subject | Recombinant Proteins | - |
dc.subject | DNA Primers | - |
dc.subject | Transfection | - |
dc.subject | Mutagenesis, Site-Directed | - |
dc.subject | Polymerase Chain Reaction | - |
dc.subject | Signal Transduction | - |
dc.subject | Cell Division | - |
dc.subject | Gene Expression Regulation | - |
dc.subject | Amino Acid Sequence | - |
dc.subject | Base Sequence | - |
dc.subject | Point Mutation | - |
dc.subject | Molecular Sequence Data | - |
dc.subject | Receptors, Interleukin-5 | - |
dc.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 | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1002/j.1460-2075.1995.tb00102.x | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Jenkins, B. [0000-0002-7552-4656] | - |
dc.identifier.orcid | Gonda, T. [0000-0002-8792-3021] | - |
Appears in Collections: | Aurora harvest 4 Medicine publications |
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