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The ras oncogene--an important regulatory element in lower eucaryotic organisms.

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The ras oncogene--an important regulatory element in lower eucaryotic organisms.
Id. 17939939
Idioma inglés
Titulo The ras oncogene--an important regulatory element in lower eucaryotic organisms.
Autor(es) Gibbs, J B
Marshall, M S
Localización http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=372726
Versión 1.0
Estado Final
Descripción The ras proto-oncogene in mammalian cells encodes a 21-kilodalton guanosine triphosphate (GTP)-binding protein. This gene is frequently activated in human cancer. As one approach toward understanding the mechanisms of cellular transformation by ras, the function of this gene in lower eucaryotic organisms has been studied. In the yeast Saccharomyces cerevisiae, the RAS gene products serve as essential function by regulating cyclic adenosine monophosphate metabolism. Stimulation of adenylyl cyclase is dependent not only on RAS protein complexed to GTP, but also on the CDC25 and IRA gene products, which appear to control the RAS GTP-guanosine diphosphate cycle. Although analysis of RAS biochemistry in S. cerevisiae has identified mechanisms central to RAS action, RAS regulation of adenylyl cyclase appears to be strictly limited to this particular organism. In Schizosaccharomyces pombe, Dictyostelium discoideum, and Drosophila melanogaster, ras-encoded proteins are not involved with regulation of adenylyl cyclase, similar to what is observed in mammalian cells. However, the ras gene product in these other lower eucaryotes is clearly required for appropriate responses to extracellular signals such as mating factors and chemoattractants and for normal growth and development of the organism. The identification of other GTP-binding proteins in S. cerevisiae with distinct yet essential functions underscores the fundamental importance of G-protein regulatory processes in normal cell physiology.
Palabras clave Research Article
Tipo de recurso Text
Tipo de Interactividad Expositivo
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Fecha de contribución 11-feb-2008
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