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首页> 外文期刊>The Biochemical Journal >Distinct roles for extracellular-signal-regulated protein kinase (ERK) mitogen-activated protein kinases and phosphatidylinositol 3-kinase in the regulation of Mcl-1 synthesis.
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Distinct roles for extracellular-signal-regulated protein kinase (ERK) mitogen-activated protein kinases and phosphatidylinositol 3-kinase in the regulation of Mcl-1 synthesis.

机译：细胞外信号调节蛋白激酶（ERK）丝裂原活化蛋白激酶和磷脂酰肌醇3-激酶在调节Mcl-1合成中的不同作用。

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摘要

Alterations in the expression of various Bcl-2 family members may act as one means by which a cell's survival may be regulated. The mechanism by which cytokines regulate expression of Bcl-2 family members was examined in the haemopoietic cell line TF-1. Cytokine-induced Mcl-1 protein expression was shown to be controlled through a pathway dependent upon phosphatidylinositol 3-kinase (PI 3-kinase). The cytokine-induced increase in mRNA transcription was not dependent upon PI 3-kinase, thus dissociating the immediate-early transcription factors responsible for Mcl-1 transcription from the PI 3-kinase signalling pathway. In contrast, Mcl-1 mRNA levels were dependent upon MEK [mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated protein kinase kinase] activation, suggesting a role for the Ras/MEK/MAPK pathway in Mcl-1 transcription. Activation of PI 3-kinase was shown to be necessary to stimulate Mcl-1 protein translation. This was not due to any effect on prolonging the half-life of the protein. Finally, the lipid second messenger ceramide was shown to cause a reduction in Mcl-1 protein translation, probably via its ability to inhibit protein kinase B activation, providing further clues regarding the death-inducing effect of this lipid.
机译：各种Bcl-2家族成员表达的改变可能是调节细胞存活的一种手段。在造血细胞系TF-1中检查了细胞因子调节Bcl-2家族成员表达的机制。细胞因子诱导的Mcl-1蛋白表达被证明是通过依赖于磷脂酰肌醇3-激酶（PI 3-激酶）的途径来控制的。细胞因子诱导的mRNA转录增加不依赖于PI 3激酶，因此从PI 3激酶信号通路中解离了负责Mcl-1转录的立即早期转录因子。相反，Mcl-1 mRNA的水平取决于MEK [丝裂原活化蛋白激酶（MAPK）/细胞外信号调节的蛋白激酶激酶]的激活，提示Ras / MEK / MAPK途径在Mcl-1转录中起作用。已证明活化PI 3-激酶对于刺激Mcl-1蛋白翻译是必需的。这不是由于延长蛋白质半衰期的任何影响。最后，脂质第二信使神经酰胺可能通过抑制蛋白激酶B活化而导致Mcl-1蛋白翻译减少，从而提供了有关该脂质诱导死亡的进一步线索。

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