Biological activity of a K-ras mutant that contains the 12R/59T/116Y mutations.
The 12R/59T/116Y mutations have been shown to confer a dominant negative activity on H-ras oncogene (H-ras 116Y). To determine whether this event is unique for H-ras, we introduced the same mutations into K-ras oncogene. This mutant, K-ras 116Y, suppressed transformed phenotypes induced by overexpression of H-ras proto-oncogene. NIH3T3 cells expressing K-ras 116Y were resistant to transformation by v-fes oncogene. Analysis of chimaeras between H- and K-ras 116Y showed that the C-terminal variable region determines the level of suppressor activity. These results suggest that these mutations are applicable to other GDP/GTP binding proteins.
Ogiso
Y
Y
Laboratory of Molecular Genetics, Hokkaido University School of Medicine, Japan.
Hwang
Y W
YW
Shih
T Y
TY
Kuzumaki
N
N
D016475:3T3 Cells; D000818:Animals; D001483:Base Sequence; D015152:Blotting, Northern; D002461:Cell Line, Transformed; D002472:Cell Transformation, Viral; D002678:Chimera; D011905:Genes, ras; D051379:Mice; D008969:Molecular Sequence Data; D009154:Mutation; D012190:Retroviridae / Q000235:genetics; D013489:Suppression, Genetic; D014162:Transfection; D014170:Transformation, Genetic