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| Original Paper |
| Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1 |
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| Alexandra Ikeguchi1, Hen-Ying Yang2, Guangxia Gao2 and Stephen P Goff2 |
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1Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA
2Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA
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Correspondence to: S P Goff, Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA
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| Abstract |
| The abi-1 gene encodes a protein that binds and is phosphorylated by the Abelson protein tyrosine kinase. Constructs expressing a full-length abi-1 cDNA, and a smaller cDNA arising from an alternatively spliced form, were generated and tested for their effect on transformation of NIH3T3 cells by the Abelson murine leukemia virus. Overexpression of both forms of the protein strongly inhibited transformation by the wild-type P160 strain of the virus, but not by the non-interacting mutant P90A strain. The inhibition required the SH3 domain of Abi-1, suggesting that a direct interaction was required for the effect. Rare breakthrough P160 transformants of the Abi-1 overexpressing lines were found to have downregulated Abi-1 protein levels by a post-transcriptional mechanism. Oncogene (2001) 20, 4926-4934. |
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| Keywords |
| Abelson murine leukemia virus; interacting protein |
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| Received 17 October 2000; revised 27 March 2001; accepted 2 April 2001 |
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| 16 August 2001, Volume 20, Number 36, Pages 4926-4934 |
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