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Mcl-1 Integrates the Opposing Actions of Signaling Pathways That Mediate Survival and Apoptosis

机译：Mcl-1整合了介导生存和凋亡的信号通路的相反作用

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摘要

Mcl-1 is a member of the Bcl2-related protein family that is a critical mediator of cell survival. Exposure of cells to stress causes inhibition of Mcl-1 mRNA translation and rapid destruction of Mcl-1 protein by proteasomal degradation mediated by a phosphodegron created by glycogen synthase kinase 3 (GSK3) phosphorylation of Mcl-1. Here we demonstrate that prior phosphorylation of Mcl-1 by the c-Jun N-terminal protein kinase (JNK) is essential for Mcl-1 phosphorylation by GSK3. Stress-induced Mcl-1 degradation therefore requires the coordinated activity of JNK and GSK3. Together, these data establish that Mcl-1 functions as a site of signal integration between the proapoptotic activity of JNK and the prosurvival activity of the AKT pathway that inhibits GSK3.
机译：Mcl-1是Bcl2相关蛋白家族的成员，而Bcl2相关蛋白家族是细胞存活的关键介质。细胞暴露于压力下会导致糖原合成酶激酶3（GSK3）磷酸化Mcl-1产生的磷酸化降解介导的蛋白酶体降解，从而导致 Mcl-1 mRNA的抑制和Mcl-1蛋白的快速破坏。在这里，我们证明了c-Jun N端蛋白激酶（JNK）对Mcl-1进行的磷酸化对于GSK3对Mcl-1的磷酸化至关重要。因此，应力诱导的Mcl-1降解需要JNK和GSK3的协同活性。在一起，这些数据确定Mcl-1充当JNK的促凋亡活性与抑制GSK3的AKT途径的生存活性之间的信号整合位点。

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