期刊
MOLECULAR CELL
卷 29, 期 3, 页码 362-375出版社
CELL PRESS
DOI: 10.1016/j.molcel.2007.12.024
关键词
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资金
- NCI NIH HHS [R37 CA46595, R37 CA046595, R37 CA046595-21] Funding Source: Medline
- NHGRI NIH HHS [HG3456, R01 HG003456] Funding Source: Medline
- NIGMS NIH HHS [R01 GM051405-12, R01 GM5105, R01 GM051405] Funding Source: Medline
The major participants of the Ras/ERK and PI3-kinase (PI3K) pathways are well characterized. The cellular response to activation of these pathways, however, can vary dramatically. How differences in signal strength, timing, spatial location, and cellular context promote specific cell-fate decisions remains unclear. Nuclear transport processes can have a major impact on the determination of cell fate; however, little is known regarding how nuclear transport is regulated by or regulates these pathways. Here we show that RSK and Akt, which are activated downstream of Ras/ERK and PI3K, respectively, modulate the Ran gradient and nuclear transport by interacting with, phosphorylating, and regulating Ran-binding protein 3 (RanBP3) function. Our findings highlight an important link between two major cell-fate determinants: nuclear transport and the Ras/ERK/RSK and PI3K/Akt signaling pathways.
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