The kinases aurora B and mTOR regulate the G1-S cell cycle progression of T lymphocytes. Academic Article uri icon

abstract

  • 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.

published proceedings

  • Nat Immunol

altmetric score

  • 0.25

author list (cited authors)

  • Song, J., Salek-Ardakani, S., So, T., & Croft, M.

citation count

  • 106

complete list of authors

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

publication date

  • January 1, 2007 11:11 AM