Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 7, Pages 3824-3828Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000718
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Funding
- National Cancer Institute of the National Institutes of Health [KO1CA099156-01]
- Curtis Hankamer Basic Research Fund
- Dan Duncan Cancer Center at Baylor College of Medicine
- National Institute of Allergy and Infectious Diseases [1RO1AI077536-01]
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T cell receptor activation inhibits expression of the E74-like factor (ELF) 4 and Kru ppel-like factor 4 genes to release naive CD8(+) T cells from their quiescent state. In this study, we show that ELF4 controls the ERKmediated proliferative response by maintaining normal levels of dual-specificity phosphatases 1 and 5 in CD8(+) T cells. In activated CD8(+) T cells, the mammalian target of rapamycin pathway inhibits ELF4 and Kru ppel-like factor 4 expression downstream of ERK and PI3K signaling. Our findings demonstrate that rapamycin could be used to modulate expression of this transcriptional network involved in cell-cycle regulation. The Journal of Immunology, 2010, 185: 3824-3828.
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