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Fer kinase sustains the activation level of ERK1/2 and increases the production of VEGF in hypoxic cells

机译：Fer激酶维持缺氧细胞中ERK1 / 2的激活水平并增加VEGF的产生

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摘要

Fer is a nuclear and cytoplasmic tyrosine kinase that is ubiquitously expressed in mammalian cells. Herein we show that Fer sustains a key signaling step in hypoxic cells. Knock-down of the Fer protein using a specific siRNA decreased the production of VEGF by the hypoxic cells. Conversely, ectopic expression of this kinase led to an elevated production of VEGF under hypoxia. At the molecular level, Fer was found to associate with ERK1/2 and this interaction was intensified under hypoxia. Moreover, Fer increased the activation levels of ERK1/2, and reducing the level of Fer, impaired the activation of ERK1/2 in hypoxic cells. Blocking the MEK-ERK1/2 signaling pathway with the MEK inhibitors U0126, or PD98059 led to the abrogation of ERK1/2 activity in hypoxic cells, an effect that was counteracted by Fer. Hence, fer sustains the activation of ERK1/2 and increases the production of VEGF in hypoxic cells, without affecting the MEK-ERK signaling pathway. (C) 2004 Elsevier Inc. All rights reserved.
机译：Fer是一种在哺乳动物细胞中普遍表达的核和细胞质酪氨酸激酶。在本文中，我们显示Fer在缺氧细胞中维持关键的信号传导步骤。使用特异性siRNA敲除Fer蛋白可降低低氧细胞产生VEGF的能力。相反，在低氧条件下，该激酶的异位表达导致VEGF的产生增加。在分子水平上，发现Fer与ERK1 / 2缔合，并且在缺氧条件下这种相互作用加剧。此外，Fer增加了ERK1 / 2的激活水平，降低了Fer的水平，从而损害了低氧细胞中ERK1 / 2的激活。用MEK抑制剂U0126或PD98059阻断MEK-ERK1 / 2信号传导途径可导致缺氧细胞中ERK1 / 2活性的丧失，这一作用被Fer抵消了。因此，fer维持缺氧细胞中ERK1 / 2的激活并增加VEGF的产生，而不会影响MEK-ERK信号通路。 （C）2004 Elsevier Inc.保留所有权利。

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