ISOC1 Modulates Inflammatory Responses in Macrophages through the AKT1/PEX11B/Peroxisome Pathway.
ISOC1 Modulates Inflammatory Responses in Macrophages through the AKT1/PEX11B/Peroxisome Pathway.
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DOI：
10.3390/molecules27185896
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发表时间：
2022-09-11
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炎症是多种生理和病理过程的基础，在形成随后的适应性免疫反应和控制病原体方面起着重要作用。然而，其生理功能尚不完全清楚。通过lps处理的RAW264.7巨噬细胞炎症模型，我们发现isoc1缺陷细胞中炎症因子的产生明显高于对照组。进一步证明，ISOC1缺乏可以激活AKT1，而AKT1的过度激活可以通过蛋白修饰降低PEX11B的稳定性，从而减少过氧化物酶体的生物发生，从而影响炎症。本研究首次报道了ISOC1在先天免疫中的作用，并阐明了ISOC1通过AKT1/PEX11B/过氧化物酶体调控炎症的机制。我们的研究结果确定了iso1在lps诱导的炎症反应的调节机制中的新作用。
Inflammation underlies a variety of physiological and pathological processes and plays an essential role in shaping the ensuing adaptive immune responses and in the control of pathogens. However, its physiological functions are not completely clear. Using a LPS-treated RAW264.7 macrophage inflammation model, we found that the production of inflammatory cytokines in ISOC1-deficient cells was significantly higher than that in the control group. It was further proved that ISOC1 deficiency could activate AKT1, and the overactivation of AKT1 could reduce the stability of PEX11B through protein modification, thereby reducing the peroxisome biogenesis and thus affecting inflammation. In this study, we reported for the first time the role of ISOC1 in innate immunity and elucidated the mechanism by which ISOC1 regulates inflammation through AKT1/PEX11B/peroxisome. Our results defined a new role of ISOC1 in the regulatory mechanism underlying the LPS-induced inflammatory response.
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影响因子：
4.4
作者：
Gilbert FB;Cunha P;Jensen K;Glass EJ;Foucras G;Robert-Granié C;Rupp R;Rainard P
通讯作者：
Rainard P
影响因子：
2.3
作者：
Angermueller, Sabine;Islinger, Markus;Voelkl, Alfred
通讯作者：
Voelkl, Alfred
可生物降解的镁基合金通过 TRPM7-PI3K-AKT1 信号轴抑制 THP-1 细胞来源的巨噬细胞的炎症反应
影响因子：
7.3
作者：
Jin, Liang;Chen, Chenxin;Chen, Tongxin
通讯作者：
Chen, Tongxin
影响因子：
4.4
作者：
Chandel, NS;Trzyna, WC;Schumacker, PT
通讯作者：
Schumacker, PT
影响因子：
4
作者：
Ebberink, Merel S.;Koster, Janet;Waterham, Hans R.
通讯作者：
Waterham, Hans R.