Answers are grounded in this paper and cite their sources.
Experimental study demonstrates that mTOR signaling downregulates ELF4 in activated CD8+ T cells, suggesting rapamycin can modulate immune cell cycle networks.
T cell receptor activation inhibits expression of the E74-like factor (ELF) 4 and Krüppel-like factor 4 genes to release naive CD8(+) T cells from their quiescent state. In this study, we show that ELF4 controls the ERK-mediated 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 Krüppel-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.
No takes yet. Share an insight, caveat, or question.
Yamada et al. (2010) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: