Oxidation as a post-translational modification that regulates autophagy
Oxidation as a post-translational modification that regulates autophagy
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DOI：
10.4161/auto.4214
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发表时间：
2007-07-01
期刊：
影响因子：
13.3
通讯作者：
Elazar, Ivulun
中科院分区：
文献类型：
--
作者：
Scherz-Shouval, Ruth;Shvets, Elena;Elazar, Ivulun
与活性氧（ROS）积累相关的毒性导致了各种防御策略的演变，以克服氧化应激，包括自噬。该途径参与受损线粒体和氧化蛋白的去除和降解。然而，在低水平下，ROS在各种细胞内途径中充当信号转导子。在最近的一项研究中，我们描述了ROS作为信号分子在饥饿诱导的自噬中的作用。我们发现，饥饿刺激ROS的形成，特别是H2O2，在线粒体中。此外，我们确定了半胱氨酸蛋白酶HsAtg4作为H2O2氧化的直接靶点，并指定了位于HsAtgA催化位点附近的半胱氨酸残基作为这种调节的关键。在这里，我们专注于Atg4，调节的目标，并讨论可能的机制，这种酶在自噬过程中的调节。
The toxicity associated with accumulation of reactive oxygen species (ROS) has led to the evolution of various defense strategies to overcome oxidative stress, including autophagy. This pathway is involved in the removal and degradation of damaged mitochondria and oxidized proteins. At low levels, however, ROS act as signal transducers in various intracellular pathways. In a recent study we described the role of ROS as signaling molecules in starvation-induced autophagy. We showed that starvation stimulates formation of ROS, specifically H2O2, in the mitochondria. Furthermore, we identified the cysteine protease HsAtg4 as a direct target for oxidation by H2O2, and specified a cysteine residue located near the HsAtgA catalytic site as critical for.this regulation. Here we focus on Atg4, the target of regulation, and discuss possible mechanisms for the regulation of this enzyme in the autophagic process.