mTORC1型
蛋白激酶B
细胞生物学
PI3K/AKT/mTOR通路
巨噬细胞极化
信号转导
生物
代谢网络
代谢途径
巨噬细胞
化学
生物化学
新陈代谢
体外
作者
Anthony J. Covarrubias,Halil‐Ibrahim Aksoylar,Jiujiu Yu,Nathaniel W. Snyder,Andrew J. Worth,Shankar S. Iyer,Jiawei Wang,Issam Ben-Sahra,Vanessa Byles,Tiffany Polynne-Stapornkul,Erika C Espinosa,Dudley W. Lamming,Brendan D. Manning,Yijing Zhang,Ian A. Blair,Tiffany Horng
出处
期刊:eLife
[eLife Sciences Publications, Ltd.]
日期:2016-02-19
卷期号:5
被引量:299
摘要
Macrophage activation/polarization to distinct functional states is critically supported by metabolic shifts. How polarizing signals coordinate metabolic and functional reprogramming, and the potential implications for control of macrophage activation, remains poorly understood. Here we show that IL-4 signaling co-opts the Akt-mTORC1 pathway to regulate Acly, a key enzyme in Ac-CoA synthesis, leading to increased histone acetylation and M2 gene induction. Only a subset of M2 genes is controlled in this way, including those regulating cellular proliferation and chemokine production. Moreover, metabolic signals impinge on the Akt-mTORC1 axis for such control of M2 activation. We propose that Akt-mTORC1 signaling calibrates metabolic state to energetically demanding aspects of M2 activation, which may define a new role for metabolism in supporting macrophage activation.
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