TY - JOUR
T1 - Multiple ras functions can contribute to mammalian cell transformation
AU - White, Michael A.
AU - Nicolette, Charles
AU - Minden, Audrey
AU - Polverino, Anthony
AU - Aelst, Linda Van
AU - Karin, Michael
AU - Wigler, Michael H.
N1 - Funding Information:
Vojtek, Stevan Marcus, and Stanley Fields for supplying some of the plasmids and yeast strains used in this study. We thank Linda Rodgers and Michael Riggs for valuable technical assistance. A. M. was supported by a postdoctoral fellowship from the Tobacco-Related Disease Research Program. L. V. A. is supported by the Belgian National Fund for Scientific Research. M. H. W. is an American Cancer Society Research Professor. This study is supported by grants from the American Cancer Society and the National Cancer Institute.
PY - 1995/2/24
Y1 - 1995/2/24
N2 - We have developed a generalized approach, using two hybrid interactions, to isolate Ha-Ras effector loop mutations that separate the ability of Ha-Ras to interact with different downstream effectors. These mutations attenuate or eliminate Ha-ras(G12V) transformation of mammalian cells, but retain complementary activity, as demonstrated by synergistic induction of foci of growth-transformed cells, and by the ability to activate different downstream components. The transformation defect of Ha-ras(G12V, E37G) is rescued by a mutant, raf1, that restores interaction. These results indicate that multiple cellular components, including Raf1, are activated by Ha-Ras and contribute to Ha-Ras-induced mammalian cell transformation.
AB - We have developed a generalized approach, using two hybrid interactions, to isolate Ha-Ras effector loop mutations that separate the ability of Ha-Ras to interact with different downstream effectors. These mutations attenuate or eliminate Ha-ras(G12V) transformation of mammalian cells, but retain complementary activity, as demonstrated by synergistic induction of foci of growth-transformed cells, and by the ability to activate different downstream components. The transformation defect of Ha-ras(G12V, E37G) is rescued by a mutant, raf1, that restores interaction. These results indicate that multiple cellular components, including Raf1, are activated by Ha-Ras and contribute to Ha-Ras-induced mammalian cell transformation.
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U2 - 10.1016/0092-8674(95)90507-3
DO - 10.1016/0092-8674(95)90507-3
M3 - Article
C2 - 7867061
AN - SCOPUS:0028948382
SN - 0092-8674
VL - 80
SP - 533
EP - 541
JO - Cell
JF - Cell
IS - 4
ER -