炎症中的自噬：p38αMAPK-ULK1轴

Macrophage Pub Date : 2018-03-09 DOI:10.14800/MACROPHAGE.1629

H. She, Yingli He, Ying‐ren Zhao, Zixu Mao

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引用次数: 4

摘要

自噬和炎症是免疫细胞发挥其功能的两个重要过程。它们在信号上的适当相互作用是对压力作出适当反应的关键。小胶质细胞中的应激激酶p38α MAPK感知炎症线索LPS，直接磷酸化ULK1，减轻对炎症机制的自噬抑制，从而允许充分的免疫反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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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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