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

Activation of CD4 T cells by Raf-independent effectors of Ras.

Small GTPase Ras is capable of mediating activation in T lymphocytes by using Raf kinase-dependent signaling pathway. Other effectors of Ras exist, however, suggesting that targets of Ras alternative to Raf may also contribute to T cell functions. Here we demonstrate that Ras(V12G37) mutant that fails to bind Raf, potently increases intracellular calcium concentration and cytokine production in primary antigen-stimulated T cells. From three known effectors which retain the ability to interact with Ras(V12G37), overexpression of phospholipase C epsilon but not that of RIN1 or Ral guanine nucleotide exchange factors enhanced cytokine and nuclear factor-activated T cell reporter T cell responses. Hence T cell activation can be critically regulated by the Ras effector pathway independent from Raf that can be mimicked by phospholipase C epsilon.[1]


  1. Activation of CD4 T cells by Raf-independent effectors of Ras. Czyzyk, J., Brogdon, J.L., Badou, A., Henegariu, O., Preston Hurlburt, P., Flavell, R., Bottomly, K. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
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