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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

RalGDS functions in Ras- and cAMP-mediated growth stimulation.

Thyroid-stimulating hormone stimulates proliferation through both the cAMP-dependent protein kinase and Ras but not through Raf-1 and mitogen-activated and extracellular signal-related kinase kinase. We now report that thyroid-stimulating hormone represses mitogen-activated protein kinase activity and that microinjection of an effector domain mutant Ha-Ras protein, Ras(12V,37G), defective in Raf-1 binding and mitogen-activated protein kinase activation, stimulates DNA synthesis in quiescent and thyroid-stimulating hormone-treated thyrocytes. A yeast two-hybrid screen identified RalGDS as a Ras(12V,37G) binding protein and therefore a potential effector of Ras in these cells. Associations between Ras and RalGDS were observed in extracts prepared from thyroid cells. Microinjection of a mutant RalA(28N) protein thought to sequester RalGDS family members reduced DNA synthesis stimulated by Ras as well as cAMP-mediated DNA synthesis in two cell lines which respond to cAMP with mitogenesis. These results support the idea that RalGDS may be an effector of Ras in cAMP-mediated growth stimulation.[1]


  1. RalGDS functions in Ras- and cAMP-mediated growth stimulation. Miller, M.J., Prigent, S., Kupperman, E., Rioux, L., Park, S.H., Feramisco, J.R., White, M.A., Rutkowski, J.L., Meinkoth, J.L. J. Biol. Chem. (1997) [Pubmed]
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