The kinases aurora B and mTOR regulate the G1-S cell cycle progression of T lymphocytes

Jianxun Song, Shahram Salek-Ardakani, Takanori So, Michael Croft

Research output: Contribution to journalArticlepeer-review

104 Scopus citations


CD28-deficient T cells arrest at the G1-S transition of the cell cycle. Here we show that this is controlled by the kinase aurora B, which exists in a complex with survivin and mammalian target of rapamycin (mTOR). Expression of aurora B in Cd28-/- T cells augmented phosphorylation of mTOR substrates, expression of cyclin A, hyperphosphorylation of retinoblastoma protein and activation of cyclin-dependent kinases 1 and 2 and promoted cell cycle progression. Interleukin 2 enhanced aurora B activity, and inactive aurora B prevented interleukin 2-induced proliferation. Moreover, expression of aurora B restored Cd28-/- T cell proliferation and promoted inflammation in vivo. These data identify aurora B, along with survivin and mTOR, as a regulator of the G1-S checkpoint in T cells.

Original languageEnglish (US)
Pages (from-to)64-73
Number of pages10
JournalNature Immunology
Issue number1
StatePublished - Jan 2007

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


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