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

Jan Czyzyk, Jennifer L. Brogdon, Abdallah Badou, Octavian Henegariu, Paula Preston Hurlburt, Richard Flavell, Kim Bottomly

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


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 RasV12G37 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 RasV12G37, over-expression of phospholipase C ε 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 ε.

Original languageEnglish (US)
Pages (from-to)6003-6008
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number10
StatePublished - May 13 2003
Externally publishedYes


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