Oncogenic ras activation of Raf/mitogen-activated protein kinase-independent pathways is sufficient to cause tumorigenic transformation
Molecular and Cellular Biology, ISSN: 0270-7306, Vol: 16, Issue: 7, Page: 3923-3933
1996
- 331Citations
- 81Captures
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Metrics Details
- Citations331
- Citation Indexes331
- 331
- CrossRef289
- Captures81
- Readers81
- 81
Article Description
Substantial evidence supports a critical role for the activation of the Raf-1/MEK/mitogen-activated protein kinase pathway in oncogenic Ras-mediated transformation. For example, dominant negative mutants of Raf-1, MEK, and mitogen-activated protein kinase all inhibit Ras transformation. Furthermore, the observation that plasma membrane-localized Raf-1 exhibits the same transforming potency as oncogenic Ras suggests that Raf-1 activation alone is sufficient to mediate full Ras transforming activity. However, the recent identification of other candidate Ras effectors (e.g., RalGDS and phosphatidylinositol-3 kinase) suggests that activation of other downstream effector-mediated signaling pathways may also mediate Ras transforming activity. In support of this, two H-Ras effector domain mutants, H-Ras(12V, 37G) and H-Ras(12V, 40C), which are defective for Raf binding and activation, induced potent tumorigenic transformation of some strains of NIH 3T3 flbroblasts. These Raf-binding defective mutants of H-Ras induced a transformed morphology that was indistinguishable from that induced by activated members of Rho family proteins. Furthermore, the transforming activities of both of these mutants were synergistically enhanced by activated Raf-1 and inhibited by the dominant negative RhoA(19N) mutant, indicating that Ras may cause transformation that occurs via coordinate activation of Raf-dependent and -independent pathways that involves Rho family proteins. Finally, cotransfection of H-Ras(12V, 37G) and H-Ras(12V, 40C) resulted in synergistic cooperation of their focus-forming activities, indicating that Ras activates at least two Raf-independent, Ras effector-mediated signaling events.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0029890896&origin=inward; http://dx.doi.org/10.1128/mcb.16.7.3923; http://www.ncbi.nlm.nih.gov/pubmed/8668210; http://mcb.asm.org/lookup/doi/10.1128/MCB.16.7.3923; https://syndication.highwire.org/content/doi/10.1128/MCB.16.7.3923; https://www.tandfonline.com/doi/full/10.1128/MCB.16.7.3923; https://dx.doi.org/10.1128/mcb.16.7.3923; https://journals.asm.org/doi/10.1128/MCB.16.7.3923; https://mcb.asm.org/content/16/7/3923; https://mcb.asm.org/content/16/7/3923.abstract; https://mcb.asm.org/content/16/7/3923.full.pdf; http://mcb.asm.org/content/16/7/3923; https://mcb.asm.org/content/mcb/16/7/3923.full.pdf
American Society for Microbiology
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