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Dissecting the role of redox signaling in neuronal development

机译:剖析氧化还原信号在神经元发育中的作用

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摘要

The generation of abnormally high levels of reactive oxygen species (ROS) is linked to cellular dysfunction, including neuronal toxicity and neurodegeneration. However, physiological ROS production modulates redox-sensitive roles of several molecules such as transcription factors, signaling proteins, and cytoskeletal components. Changes in the functions of redox-sensitive proteins may be important for defining key aspects of stem cell proliferation and differentiation, neuronal maturation, and neuronal plasticity. In neurons, most of the studies have been focused on the pathological implications of such modifications and only very recently their essential roles in neuronal development and plasticity has been recognized. In this review, we discuss the participation of NADPH oxidases (NOXs) and a family of protein-methionine sulfoxide oxidases, named molecule interacting with CasLs, as regulated enzymatic sources of ROS production in neurons, and describes the contribution of ROS signaling to neurogenesis and differentiation, neurite outgrowth, and neuronal plasticity.
机译:异常高水平的活性氧(ROS)的产生与细胞功能障碍有关,包括神经元毒性和神经变性。但是,生理性ROS的产生可调节几种分子(例如转录因子,信号蛋白和细胞骨架成分)的氧化还原敏感作用。氧化还原敏感蛋白功能的变化对于定义干细胞增殖和分化,神经元成熟和神经元可塑性的关键方面可能很重要。在神经元中,大多数研究都集中在此类修饰的病理意义上,直到最近才认识到它们在神经元发育和可塑性中的重要作用。在这篇综述中,我们讨论了NADPH氧化酶(NOXs)和蛋白质-蛋氨酸亚砜氧化酶家族的参与,该分子称为与CasLs相互作用的分子,作为神经元中ROS产生的调控酶源,并描述了ROS信号对神经发生和形成的贡献。分化,神经突生长和神经元可塑性。

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