Cytoprotective mechanisms of DJ-1 against oxidative stress through modulating ERK1/2 and ASK1 signal transduction.
Cytoprotective mechanisms of DJ-1 against oxidative stress through modulating ERK1/2 and ASK1 signal transduction.
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DOI：
10.1016/j.redox.2017.09.008
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发表时间：
2018-04
期刊：
影响因子：
11.4
通讯作者：
Mouradian MM
中科院分区：
文献类型：
--
作者：
Oh SE;Mouradian MM
DJ-1是一种高度保守的多功能蛋白质，与神经退行性变和肿瘤形成有关。在其各种活动中，有一种抗氧化特性，可在氧化应激条件下产生细胞保护作用。这与调节信号转导事件的能力有关，信号转导事件决定细胞如何调节正常过程，如生长，衰老，凋亡和自噬，以适应环境刺激和压力。DJ-1表达或功能的改变可以破坏稳态信号网络，并启动级联反应，在帕金森病和癌症等疾病的发病机制中发挥作用。DJ-1在多种信号通路中起重要作用。与其抗氧化特性相关，它通过激活细胞外信号调节激酶（ERK 1/2）途径介导细胞存活和增殖，并通过抑制凋亡信号调节激酶1（ASK 1）激活来减弱细胞死亡信号。在这里，我们回顾了DJ-1调节这些途径的方式，重点是如何调节信号转导有助于细胞内稳态和病理状态，导致其失调。
DJ-1 is a highly conserved multifunctional protein linked to both neurodegeneration and neoplasia. Among its various activities is an antioxidant property leading to cytoprotection under oxidative stress conditions. This is associated with the ability to modulate signal transduction events that determine how the cell regulates normal processes such as growth, senescence, apoptosis, and autophagy in order to adapt to environmental stimuli and stresses. Alterations in DJ-1 expression or function can disrupt homeostatic signaling networks and initiate cascades that play a role in the pathogenesis of conditions such as Parkinson's disease and cancer. DJ-1 plays a major role in various signaling pathways. Related to its anti-oxidant properties, it mediates cell survival and proliferation by activating the extracellular signal-regulated kinase (ERK1/2) pathway and attenuates cell death signaling by inhibiting apoptosis signal-regulating kinase 1 (ASK1) activation. Here, we review the ways through which DJ-1 regulates these pathways, focusing on how its regulation of signal transduction contributes to cellular homeostasis and the pathologic states that result from their dysregulation.
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