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首页> 外文期刊>Nature >Bmk1/Erk5 is required for cell proliferation induced by epidermal growth factor.
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Bmk1/Erk5 is required for cell proliferation induced by epidermal growth factor.

机译：Bmk1 / Erk5是表皮生长因子诱导的细胞增殖所必需的。

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摘要

Epidermal growth factor (EGF) induces cell proliferation in a variety of cell types by binding to a prototype transmembrane tyrosine kinase receptor. Ligation of this receptor by EGF activates Erk1 and Erk2, members of the mitogen-activated protein (MAP) kinase family, through a Ras-dependent signal transduction pathway. Despite our detailed understanding of these events, the exact mechanism by which EGF causes cells to proliferate is unclear. Big MAP kinase (Bmk1), also known as Erk5, is a member of the MAP kinase family that is activated in cells in response to oxidative stress, hyperosmolarity and treatment with serum. Here we show that EGF is a potent activator of Bmk1. In contrast to Erk1/2, EGF-mediated activation of Bmk1 occurs independently of Ras and requires the MAP-kinase kinase Mek5. Expression of a dominant-negative form of Bmk1 blocks EGF-induced cell proliferation and prevents cells from entering the S phase of the cell cycle. These results demonstrate that Bmk1 is part of a distinct MAP-kinase signalling pathway that is required for EGF-induced cell proliferation and progression through the cell cycle.
机译：表皮生长因子（EGF）通过与原型跨膜酪氨酸激酶受体结合来诱导多种细胞类型的细胞增殖。 EGF对该受体的连接通过Ras依赖性信号转导途径激活有丝分裂原活化蛋白（MAP）激酶家族成员Erk1和Erk2。尽管我们对这些事件有详尽的了解，但EGF引起细胞增殖的确切机制尚不清楚。大MAP激酶（Bmk1），也称为Erk5，是MAP激酶家族的成员，可在细胞中被激活，以响应氧化应激，高渗性和血清治疗。在这里，我们证明EGF是Bmk1的有效激活剂。与Erk1 / 2相反，EGF介导的Bmk1激活独立于Ras发生，需要MAP激酶激酶Mek5。 Bmk1显性阴性形式的表达可阻止EGF诱导的细胞增殖，并阻止细胞进入细胞周期的S期。这些结果表明Bmk1是EGF诱导的细胞增殖和细胞周期进展所需的独特MAP激酶信号通路的一部分。

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