ArticleMolecular and cellular biology1997
Interaction of activated Ras with Raf-1 alone may be sufficient for transformation of rat2 cells.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- The RAS effector RIN1 directly competes with RAF and is regulated by 14-3-3 proteins.Molecular and cellular biology · 2002Article
- Cyclic AMP-mediated inhibition of cell growth requires the small G protein Rap1.Molecular and cellular biology · 2001Article
- Article
- Signals from the Ras, Rac, and Rho GTPases converge on the Pak protein kinase in Rat-1 fibroblasts.Molecular and cellular biology · 1999Article
- Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.Genes & development · 1998Article
- Differential effects of protein kinase A on Ras effector pathways.Molecular and cellular biology · 1998Article
- Ras signals to the cell cycle machinery via multiple pathways to induce anchorage-independent growth.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
v-H-ras effector mutants have been assessed for transforming activity and for the ability of the encoded proteins to interact with Raf-1-, B-Raf-, byr2-, ralGDS-, and CDC25-encoded proteins in the yeast two-hybrid system. Transformation was assessed in rat2 cells as well as in a mutant cell line, rv68BUR, that affords a more sensitive transformation assay. Selected mutant Ras proteins were also examined for their ability to interact with an amino-terminal fragment of Raf-1 in vitro. Finally, possible cooperation between different v-H-ras effector mutants and between effector mutants and overexpressed Raf-1 was assessed. Ras transforming activity was shown to correlate best with the ability of the encoded protein to interact with Raf-1. No evidence for cooperation between v-H-ras effector mutants was found. Signaling through the Raf1-MEK-mitogen-activated protein kinase cascade may be the only effector pathway contributing to RAS transformation in these cells.
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