Laboratory of Gene Regulation and Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Mol Cell. 2012 Jun 29;46(6):717-9. doi: 10.1016/j.molcel.2012.06.001.
In this issue of Molecular Cell, Yanagiya et al. (2012) describe a regulatory mechanism that couples the abundance of the translational repressor 4E-BP1 with its target eIF4E via proteasomal degradation of 4E-BP1, thus maintaining translation in cells depleted of eIF4E.
在本期《分子细胞》中，Yanagiya 等人（2012）描述了一个调控机制，通过蛋白酶体降解 4E-BP1 将翻译抑制剂 4E-BP1 的丰度与其靶标 eIF4E 偶联起来，从而在 eIF4E 耗竭的细胞中维持翻译。
