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

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.

authors

• Song, Jianxun

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 2007

publisher

• Springer Nature  Publisher

published in

• Nature Immunology  Journal

keywords

• Animals
• Aurora Kinase B
• Aurora Kinases
• Cd28 Antigens
• Cells, Cultured
• G1 Phase
• Inhibitor Of Apoptosis Proteins
• Mice
• Mice, Transgenic
• Microtubule-Associated Proteins
• Protein Kinases
• Protein Serine-threonine Kinases
• Receptors, Interleukin-2
• Repressor Proteins
• S Phase
• Signal Transduction
• Survivin
• T-Lymphocytes
• TOR Serine-Threonine Kinases

Digital Object Identifier (DOI)

• 10.1038/ni1413

start page

• 64

end page

• 73

volume

• 8

issue

• 1

URL

• http://dx.doi.org/10.1038/ni1413