首页> 美国卫生研究院文献>The Journal of Biological Chemistry >T-LAK Cell-originated Protein Kinase (TOPK) Phosphorylation of MKP1 Protein Prevents Solar Ultraviolet Light-induced Inflammation through Inhibition of the p38 Protein Signaling Pathway
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T-LAK Cell-originated Protein Kinase (TOPK) Phosphorylation of MKP1 Protein Prevents Solar Ultraviolet Light-induced Inflammation through Inhibition of the p38 Protein Signaling Pathway

机译:T-LAK细胞起源的蛋白激酶(TOPK)的MKP1蛋白磷酸化通过抑制p38蛋白信号传导途径防止太阳紫外线诱导的炎症。

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摘要

Solar UV radiation is a major environmental factor that causes DNA damage, inflammation, and even skin cancer. T-LAK cell-originated protein kinase (TOPK) is expressed widely in both normal and cancer cells and functions to inhibit apoptosis and promote carcinogenesis. However, its function in inflammation is not known. The p38 MAPK signaling pathway plays an important role in solar UV light-induced inflammation. In this study, we found that TOPK negatively regulated the activity of p38α by phosphorylating the p38α-specific phosphatase MKP1 and enhancing the stability of MKP1. Notably, the absence of TOPK in mice resulted in a striking increase in skin inflammation. Therefore, we conclude that TOPK has a protective function in solar UV light-induced inflammation.
机译:太阳紫外线辐射是导致DNA损伤,发炎甚至皮肤癌的主要环境因素。 T-LAK细胞起源的蛋白激酶(TOPK)在正常细胞和癌细胞中广泛表达,并具有抑制细胞凋亡和促进癌变的作用。然而,其在炎症中的功能尚不清楚。 p38 MAPK信号通路在太阳紫外线引起的炎症中起重要作用。在这项研究中,我们发现TOPK通过磷酸化p38α特异性磷酸酶MKP1并增强MKP1的稳定性来负调控p38α的活性。值得注意的是,小鼠中不存在TOPK导致皮肤炎症显着增加。因此,我们得出结论,TOPK在太阳紫外线引起的炎症中具有保护功能。

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