Springer Online Journal Archives 1860-2000
Summary Mammalianras genes may naturally acquire oncogenic transformation potential through some point mutations which result in the impairment of the normalras protein functions, and which are localised in codons 12, 13 or 61. Mutationally activatedras alleles were found in a wide variety of human and carcinogen (including radiation)-induced animal malignancies. In man, myeloid leukemias are often associated with the presence of a mutationally activatedras gene (for review, see Bos JL (1989), Cancer Res 49:4682–4689). However, we failed till now in our attempts to detect oncogenicras mutations in radiation-induced mouse myeloid leukemias. We thus have the feeling thatras might perhaps participate to tumorigenesis through another mechanism provoking a deregulation of theras protein functions. In order to help evaluate such a possibility, we give here a very concise overview of the properties of theras proteins and of their regulation by a variety of still hypothetical molecular switches. This overview does not include bibliographic references. Indeed, we gathered much of the information described below at the Cold Spring Harbor Symposium on “Function and Evolution ofras Proteins”, May 9–13, 1990. Communications presented at Cold Spring Harbor Symposia may contain preliminary data and should not be cited in bibliographies. Another voluntary omission in this overview is that, for the sake of simplicity, we do not mention whether the data were obtained from experiments performed on H-, K- or N-ras. Details can be found in the published book of abstracts.
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