炎症中的自噬：p38α MAPK-ULK1 轴。

Macrophage Pub Date : 2018-01-01 Epub Date: 2018-03-09

Hua She, Yingli He, Yingren Zhao, Zixu Mao

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引用次数: 0

摘要

自噬和炎症是免疫细胞发挥其功能的两个重要过程。自噬和炎症是免疫细胞发挥其功能的两个重要过程，它们在发出信号后的适当相互作用是对应激做出适当反应的关键。小胶质细胞中的应激激酶 p38α MAPK 感受到炎症线索 LPS 后，直接使 ULK1 磷酸化，解除自噬对炎症机制的抑制，从而使免疫反应得以全面展开。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Autophagy in inflammation: the p38α MAPK-ULK1 axis.

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Autophagy in inflammation: the p38α MAPK-ULK1 axis.

Autophagy and inflammation are two processes vital for immune cells to perform their functions. Their proper interplay upon signal is pivotal for proper response to stress. The stress kinase p38α MAPK in microglia senses inflammatory cue LPS, directly phosphorylates ULK1, relieves the autophagic inhibition on the inflammatory machinery, and thus allows for a full immune response.

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Macrophage

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