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Abstract

Oncogenic activation of the proto-oncogene c- abl in human leukemias occurs as a result of the addition of exons from the gene bcr and truncation of the first abl exon. Analysis of tyrosine kinase activity and quantitative measurement of transformation potency in a single-step assay indicate that variation in bcr exon contribution results in a functional difference between p210bcr-abl and p185bcr-abl proteins. Thus, foreign upstream sequences are important in the deregulation of the kinase activity of the abl product, and the extent of deregulation correlates with the pathological effects of the bcr-abl proteins.

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References

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Science
Volume 247 | Issue 4946
2 March 1990

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Published in print: 2 March 1990

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Tracy G. Lugo
Department of Microbiology and Molecular Biology Institute and the Howard Hughes Medical Institute, University of California, Los Angeles, CA 90024.
Ann-Marie Pendergast
Department of Microbiology and Molecular Biology Institute and the Howard Hughes Medical Institute, University of California, Los Angeles, CA 90024.
Alexander J. Muller
Department of Microbiology and Molecular Biology Institute and the Howard Hughes Medical Institute, University of California, Los Angeles, CA 90024.
Owen N. Witte
Department of Microbiology and Molecular Biology Institute and the Howard Hughes Medical Institute, University of California, Los Angeles, CA 90024.

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