期刊
NATURE IMMUNOLOGY
卷 8, 期 1, 页码 64-73出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1413
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- NIAID NIH HHS [AI49453, AI50498] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI049453, P01AI050498] Funding Source: NIH RePORTER
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.
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